Kidney

Effect of Blood loss: Neurological system:

Epi and noreepi released as chemical messengers and to coordinate reflexes so the body can compensate quickly for any blood loss. for example recall that the baroreceptors located in the aortic arch and carotid arteries sense a fall in arterial pressure. sensory impulses are sent to the medulla oblongotta. the medulla oblogotta  houses both cardio axillary and inhibitory centres thereby being able to control and modulate the sympathetic response over the parasympathetic responses.  this results in an increase in heart rate and contractility by direct innervation to the heart, and cardiac output is increased. sympathetic activation ensures that this expected increase in cardiac output is diverted away from less important organs like the gut to more important organs like the brain and the heart. epinephrine and norepinephrine are released both as neurotransmitters and as hormones their effects are to increase heart rate and contractility and cause vasoconstriction and in order to maintain blood pressure and perfusion.  have you ever wondered why the carotid arteries are laced with so many receptors ? is because it's the main artery bringing blood to the brain blood loss is acute and rapid and compensatory mechanisms are no longer able to maintain perfusion to the brain neurological changes like anxiety progressing to confusion and then loss of consciousness and then possibly coma may be noted or present

Effect of Blood loss: Cardiac

Initially cardiovascular system response to blood loss by increasing heart rate increasing myocardial contractility and constricting peripheral blood vessels. this is a result of the baroreceptors sensing a change in pressure due to blood loss blood pressure may be maintained.  but if the bleeding continues profusion to the heart itself will be compromised as a workload gets progressively higher if bleeding continues to a point of reduced blood flow to organs this can lead to systemic acidosis which will get picked up by the chemoreceptors that further the sympathetic response. since vasoconstriction occurs peripherally and whatever blood flow is available is redistributed away from skin the patient will appear cool clammy and pale with an increasingly thready weak pulse before hypotension becomes more evident

Effect of blood loss Respiratory

The release if Epi by The sympathetic nervous system will cause smooth muscles in the Airways to relax causing bronchodilation an increasing respiratory rate.  this problem is further exacerbated as blood flow and perfusion to organs become reduced due to both vasoconstriction and hypoxemia. cells having to resort to anaerobic metabolism in order to generate ATP produce lactic acid and as hemorrhage persists and the more lactic acid builds up in the body systemic metabolic acidosis occurs. recall that chemo receptors also located in the Arctic branch and carotid arteries sense changes in pH and so a drop in pH will activate neural pathways to an from the respiratory centres in the brain in order to increase respiratory rate and attempt to reduce acidity by blowing off CO2

Effects of blood loss: Renal

U/O is decreased to Maintain intervascular volume. this is done by two mechanisms: one that increases circulating antidiuretic hormone by reabsorbing water and sodium in the kidneys. this is done in response to a decrease in sodium concentration sensed by osmo receptors in the brain. the other mechanism is the RAAS system when renal blood flow is reduced the kidneys agreed increased levels of renin which leads to a subsequent increase in angiotensin 2 an aldosterone. angiotensin 2 causes vascular constriction raising blood pressure and aldosterone specifically increases renal reabsorption of sodium and water.

Effects of Blood loss: GI

The pt.  a may not have clinical signs which may or may not be accompanied by different onsets and qualities of pain sensation. accumulation of blood in the GI tract is irritating and can increase peristalsis. visible peristalsis with visible signs of bleeding such as vomiting blood or the passage of bright red blood per rectum is also a very serious condition

Classes of Blood loss

As the level of shock increases so does the volume and percentage of blood loss. the following trends to notice our blood pressure decreases as bleeding continues. while heart rate increases in maintaining cardiac output as haemorrhage worsens urine output will decrease because of hypoperfusion to the kidneys. respiratory rates increasingly escalate as well due to the buildup of lactic acid as a by-product of anaerobic metabolism.  

Class 1: the body is essentially able to maintain homeostasis. \

in Class 2: some tachycardia emerges

 in class 3: hypotension accompany the tachycardia

in class 4: there is worsening of all vital signs. the patient is lethargic if not unresponsive at this stage so now

 we cannot solely rely on blood pressure as the main indicator of shock and instead we must pay attention to all of the physical assessment as a whole

Assess Severity of the bleed:

Collecting history from the patient themselves or from close family members can be vital for the team to determine the possible causes of the bleed.  internal bleeding may not be as obvious as an external cause of blood loss because patients may present with subtle signs such as weakness, lethargy, and changes in LOC. on the other hand paying close attention to the chronology and frequency of vomiting. Hematemesis, Melena, or the presence of frank red blood per rectum is important.  For example a patient who presents with vomiting frank red blood after bouts of forceful non bloody retching is more likely to have a tear at their esophageal junction referred to as a Mallory Weiss tear,  whereas a patient with a history of vomiting frank red blood from the start with complaints of acid reflux and epigastric pain are more likely to have peptic ulcer disease.

 Symptoms of diaphoresis, dyspnea, Light-headedness, and orthostatic hypotension could suggest a slower more chronic bleed or patients who are experiencing hypovolemia in larger and quicker onset bleeds.  

Also, there are specific risk factors an underlying conditions associated with GI bleeds these include: smoking, peptic ulcer disease, liver disease, coagulopathies,  alcohol abuse, excessive non-steroidal, anti-inflammatory drug use,  and conditions where people are continuously coughing and vomiting, review of NAIDS and steroid use including dose frequency and duration is important to determine the risk.

 Risk factors:

the most common risk factors for GI bleeds include gastritis, Esophageal varices /liver disease, inflammation cancer or previous history of GI bleed

 gastritis:  inflammation of the stomach lining may result in bleeding when there is an inability of the gastric lining to protect itself from gastric acids.  some causes of this include excessive NSAID, steroids, alcohol, smoking, burns or trauma.

 esophageal varices: these are swollen veins of the esophagus or stomach because of liver disease which impairs venous drainage and increases venous pressures resulting in bulging veins inflammation. may cause a breakdown of mucous membranes, if that breakdown is deep enough it may result in ulceration and bleeding.

 Cancer:  tumors disrupting the lining of the GI tract may also cause bleeding

previous GI bleed:  as most bleeds will rebleed at the same site.

 as we mentioned earlier monitoring trends in laboratory findings and results are important because they could help identify severity of blood loss the effectiveness of treatment and the discovery of an underlying cause of bleeding.

Coagulation factors: PT, PTT, Platelets, INR

 monitoring by coagulopathy by checking the prothrombin time PT, activated partial thromboplastin time PTT, and international normalized ratio INR is important both in the determination of possible cause and treatment in a patient experiencing a bleed.  for example, prolonged prothrombin time and partial thromboplastin time is prevalent in patients with liver disease or cirrhosis or patients who are prescribed long term anticoagulation and patients may require platelet transfusion and fresh frozen plasma to replace lost clotting factors when platelet counts are below 50.

BUN: urea: waste product of the digestion of protein; Bun: measures amount of urea nitrogen in the blood.

BUN, this is a by-product of the liver breaking down proteins from food that has normally been digested and what the kidneys would normally flush out if working properly. what would you expect the BUN to be in a person who is experiencing a severe GI bleed? would it be high or low? keep in mind that blood is full of protein and if there's a significant amount of blood spilling into the gut with a simultaneous drop in kidney function due to hyper perfusion, BUN levels would be high and a low GFR caused by hyperperfusion is not able to flush out this by-product plus there's an increase in BUN  production as blood is being digested along the GI tract

Hemoglobin and Hematocrit:
 Hemoglobin is an iron containing compound and is the main protein that makes up red blood cells. it allows for oxygen and carbon dioxide to bind to it so that it can be transported throughout the body.  hematocrit identifies the proportion by volume of red blood cells in relation to the total blood volume, normally this amounts to 40% in men and 31% in women. hemoglobin and hematocrit values may not accurately reflect blood loss immediately after an acute blood loss, this is because red blood cells are being lost at the same time and in the same proportion to plasma until compensatory mechanisms kick in and plasma moves from the extravascular to the intervascular space to replace volume last which at this point drops into. hemoglobin and hematocrits can be monitored and noted this redistribution of plasma can happen anywhere between 8 and 12 hours depending on how acute the bleed is. the hemoglobin and hematocrit may be deceptively low due to hemodilution. This is why monitoring the trend of hemoglobin levels and hematocrit levels along with clinical presentation is very important in assessing and evaluating the severity of the bleed.

 An unstable haemoglobin level confirms ongoing hemorrhage and will prompt further intervention from the interprofessional team. patient has acute blood loss transfusion will not be decided on the current hemoglobin alone but in consideration of the predicted drop of hemoglobin based on blood loss and the patient's clinical status. in summary, in someone who may be bleeding significantly, normal hemoglobin an hematocrit values could be measured upon admission or based on values may remain unchanged until 8 to 12 hours after redistribution of plasma occurs. but a person who is bleeding slowly over the course of a day or two may present with a very low hematocrit yet no real change in vitals as their other compensatory mechanisms are just enough to maintain vital hemostasis.

Stage 2: Stabilizing patient and controlling bleeding

GI bleed classifications: GI bleeds occurs from the upper or the lower GI tract. the ligament of treitz is located between the duodenum and the jejunum. it is an anatomical division point used to differentiate between the upper and lower GI bleeds. because bleeding below the ligament of treitz seldom, results in vomiting blood and so recognizing clinical presentations of GI bleeds can help to determine the location therefore directing further diagnostics and treatment.  Regardless of cause we're likely to see the following in the presence of a GI bleed. Hematemesis is bright frank blood in the NG tube or vomit- it's bright because it's had little time to mix with gastric secretions.  Coffee ground emesis is old digested blood gastric acid curdles the blood by converting bright red hemoglobin to brown Hematin- giving it that coffee ground grainy texture and appearance. Melena is dark tarry sticky and foul smelling stool that is a result of blood digestion in the GI tract. Hematochezia is a passage of bright red blood per rectum. an Occult bleeding is when blood is found in the stool it appears as blood streaked stool.

 These presentations can help give an idea as to where the bleed is occurring. any vomiting of blood likely indicates an upper GI source of bleeding. below the ligament of treatz seldom results in vomiting of blood. Melena can be a sign of either an upper or lower GI bleed but it is mainly associated with upper GI bleeds it depends on how long and how much blood has been exposed to gastric contents along the length of the GI tract. Menatochezia is usually associated with lower GI bleeds as the blood has not had much exposure to the digestion by the GI tract but occasionally it can also be indicative of a rapid upper GI bleed as blood quickly passes through the GI tract. this is in part due to the accumulation of blood which irritates the inner lining of the gut all causing increased peristalsis. Bright red blood or maroon stools per rectum is usually associated with lower GI bleeding

The prime consideration in a acutely ill patient with a GI bleed is to establish hemodynamic stability as quickly as possible.

 the initial treatment of GI bleeding will depend on several factors:

 including the amount of blood loss, the time frame of the blood loss, patients response to the blood loss, and underlying medical conditions or comorbidities.  in addition, the amount of blood loss is an indication of the possibility of a rebleed after treatment. with large blood loss is being more likely to rebleed than small blood losses.

 stabilization of the patient involves controlling active bleeding, treating hypovolemia, protecting the airway, and will likely involve starting adjunctive therapies.

 primary management of a GI bleeding patient begins with CAB: circulation, airway, and breathing.

 Circulation: fluid resuscitation by the interprofessional team begins immediately to stabilize the unstable patient and maintain adequate systemic perfusion. establishing good IV access can be difficult in someone experiencing hypovolemic shock but at least two large 4 IV catheter should be inserted or prepare for a central line insertion as directed by the interprofessional team. based on clinical factors the estimated blood loss and the hemoglobin, the resuscitation may include transfusion of blood products. don't forget that your type and screen should be completed with initial blood work so that crossmatching is available in case transfusing blood products is indicated.  based on the severity of the bleed, any abnormalities in coagulation tests should be corrected rapidly by either transfusing platelets or FPS as per the treating physician orders. the patient will likely be connected to the cardiac monitor and obtaining a 12 lead ECG so that any arrhythmias can be detected. the loss of the blood volume will affect the pump of the body and arrhythmias are common. careful monitoring of temperature and maintenance of normothermia is important during rapid fluid resuscitation as hypothermia can interfere with coagulation. hypothermia contributes to the loss of platelets and coagulation factor activity and can actually increase blood loss by 16% for every 1 degree Celsius it has dropped.  warming of fluids may be required as a result. additionally cold blood has shown to induce cardiac arrhythmias, particularly when it's infused too quickly. Foley insertion is vital to assess and evaluate fluid status and kidney perfusion.

airway and breathing:

 an Ng tube likely will be inserted especially if the bleed is massive the insertion is to allow for decompression of the stomach contents preventing the risk of aspiration and allows nurses to assess or rate an amount of bleeding more accurately. if there is any decreased level of consciousness or massive amounts of hematemesis,  the airway must be secured and you may need to prepare for intubation. this will prevent aspiration and allow effective oxygenation and ventilation. diagnostic and therapeutic procedures will help to determine the cause and a way to control or stop the bleeding. urgent endoscopy can be completed for high-risk patients. if patients are at lower risk that endoscopy is usually performed within 24 hours this will determine the cause and can facilitate therapeutic procedures to control or stop the bleeding.

Stabilizing Patient: Fluid therapy

The type of fluids is based on the severity of the bleed. As you can see from the table, fluid resuscitation to replace volume can be done with crystalloids, colloids, and blood products. Administering blood is dependent on the level of shock, and this is closely monitored by assessing hemodynamic status, physical signs, and symptoms and following trends in blood work. hemoglobin is generally maintained at a level above 70 unless patients with comorbidities such as coronary artery disease require higher levels of hemoglobin.  it's important to be mindful that assessing hemoglobin and hematocrit levels in isolation can be deceiving as lower levels may result from haemodilution from fluid replacement therapy or may not accurately represent the blood that's been lost as plasma will move into the intravascular space to compensate for volume lost.  once the patients hemodynamic status has been stabilized and the location or site of the bleed is determined the patient will most likely be scheduled for an endoscopy or colonoscopy.

Medication used:

Common medication include:

- the initiation of a proton pump inhibitor an example of this would be pantoprazole, anything ending in zole, all these medications reduce gastric acid secretion in order to prevent further bleeding.

 - prokinetic agents are sometimes given prior to endoscopy in the presence of a suspected upper GI bleed. they will help to facilitate gastric emptying up the routine blood and improve visibility during the scope (erythromycin or metoclopramide).

-  if there is a high suspicion or a confirmed variceal bleed octreotide can be added as a continuous infusion, it is a synthetic version of somatostatin and has selective vasoconstricting properties particularly with splenic circulation. this will reduce splenic blood flow and result in decrease portal and variceal pressures.

3) Find the cause and fix the bleed:

 most often you'll be preparing your patient for endoscopy to confirm site and help determine the appropriate therapeutic management an endoscopy is used to visualize and examine the GI tract to diagnose and can potentially be used to fix the cause of the GI bleed. once the location of the cause of the bleed is identified therapeutic procedures and interventions can be performed to fix in stop the bleed these procedures can be an endoscopic, surgical, pharmalogical or balloon tamponade therapy.

Common causes of Bleed:

Upper: causes of GI bleeds upper GI bleeding is more common than lower GI bleeding.

 three of the main causes of upper GI bleeds include: peptic ulcer disease which accounts for 50 to 75% of all upper GI cases. stress related ulcers which develop after periods of extreme physiological stress as seen in the acutely and critically ill Asafa jilan gastric varices which account for 10 to 15% upper GI bleeds but have a high mortality rate associated with them lower GI bleeds are not typically life threatening and can be caused by range of disease processes these processes can be inflammatory infectious related to pathogens or can be caused by diverticulitis hemorrhoids or even tumors

Peptic Ulcer: it accounts for 20% of all GI bleeds and about 50 to 75% of all upper GI bleeds this includes the ulceration of the stomach as well as the ulceration of the duodenum. however duodenal ulcers are more common. normally epithelial cells in the stomach produce acidic gastric juices made-up of acids and enzymes to help breakdown chyme the hydrochloric acid produced by parietal cells. a second degree burn if exposed to the skin specialized cells that align the epithelial walan Brunner glands within the mucosa work in a coordinated effort to increase pH by producing bicarbonate. a layer of mucus is also produced by cells lining. the gastric pits to protect the epithelial cell layer from the erosion not only caused by gastric juices but also caused by medications, alcohol, smoking, and bacteria and also forms when there's a disruption in the balance between these two mechanisms. if the epithelial wall becomes eroded the blood vessels in the lamina propria become vulnerable to injury leading to bleeding. blood vessels the severity of the bleed could escalate quickly into shock.

Stress related mucosal disease: they are very well documented and are found specifically in the acutely and critically ill patients who are experiencing episodes of high physiological stress the pathology is similar to that of peptic ulcer disease but the cause is related to hyperperfusion and ischaemia of the GI tract this means that when the patient is under stress their sympathetic nervous system is activated and blood is diverted away from the gut this causes an imbalance because the mucosal defence mechanism breaks down and the gastric acid penetrates the gut wall leading to destruction and erosion. this can even cause an opening of a blood vessel allowing free flow of blood into the gut. stress ulcers can develop within hours of admission to the step down unit or ICU some examples of conditions that promote higher levels of physiological stress are extensive burns, severe trauma, major surgery shock, sepsis or acute neurologic disease.

 but there are two independent risk factors that have been linked to the development of stress ulcers: mechanical ventilation for longer than 48 hours and Coagulopathy. this is important to know because there are specific strategies to prevent stress ulcers developing in the acute and critical care environments: feeding as soon as possible is one of them this is important because it provides good nutrition and energy increases pH thereby minimizing acid injury and increases blood flow to help support the mucosal barrier and ensuring the epithelial layer is regenerated with new cells. another is initiating a proton pump inhibitor like pantoloc or a histamine 2 receptor blocker such as from auditing and rigidity this will help to directly lower acidity in the stomach

Gastroesophageal Varices: emergency and it requires quick intervention as it has a 20 to 30% mortality rate associated with each bleeding episode. It refers to the swollen veins of the esophagus as a result of portal hypertension when blood cannot flow easily through the liver due to an obstructive disease like cirrhosis. where there's a lot of scar tissue blood flow is forced into other channels and is diverted into smaller low pressure veins that are not used to carrying such large volumes of blood. these veins become engorged and are vulnerable to damage from gastric secretions possibly rupturing and spewing out blood. patients with non cirrhosis will be carefully monitored for portal hypertension and to monitor the status of their gastro oesophageal varices through routine endoscopes.

Inflammatory bowel disease: 2 common types are ulcerated colitis and Crohn's disease. both cause inflammation and destruction of the mucosa in the GI tract. ulcerated colitis is limited to the large intestine however Crohn's can occur anywhere within the GI tract. in both cases an inflammatory response is triggered eventually leading to cellular damage of the epithelial lining of the GI tract this may cause ulcers to form and these ulcers may bleed in ulcerated colitis the ulcers generally extend to the submucosa but in Crohn's disease these ulcers may be quite deep extending through the entire depth of the mucosal wall

Pathogens: overgrowth of this bacteria or introduction of others may damage the GI tract one such example is E-coli strains of this bacteria can be found naturally in the gut or contributes to maintaining the balance and gut flora but virulent strains of this. bacteria can cause necrosis in the bowel one specific strain of E coli is known to produce a potent cytotoxin that damages the tissue of the large intestine leading to a rapidly evolving bloody diarrhea. strain is mainly associated with undercooked beef and can spread person to person upon contact it causes nausea and vomiting and bloody diarrhea

Diverticulitis: the large intestine has pouches called diverticula that develop in the lining these pouches lead to complications such as diverticulitis. where the diverticula are inflamed or infected due to stool getting trapped inside them. this inflammatory process may damage the epithelial lining of the colon and result in bleeding.

GI bleeds confirmed by endoscopy. But treatments may vary on the cause. for example, peptic ulcers can be treated with direct thermal therapy or heat cauterizes the bleeding vessel or other agents like hypertonic saline, epinephrine an ethanol can be injected at the site to vasoconstrict blood vessels. however sclerotherapy is the most common form of endoscopy treatment. it injects a bleeding ulcer with a necrotizing agent decreasing blood flow almost immediately. - in the case of varices, banding is commonly done this is known as endoscopic variceal ligation sometimes patients can also get a transjugular intrahepatic portosystemic stent shunt also known as a TIPS procedure. this place is a stent in the portal vein to hopefully decrease the pressure back up and decrease the likelihood of those varices blowing. if you're dealing with a massive bleed let's say from variceal bleeding balloon tamponade therapy can be done to emergently control bleeding with the placement of a Sengtaken-Blakemore (SB tube) tube. prior to using this balloon tamponade therapy the patient must be integrated to protect their airway therefore they will be in the ICU. the SB tube is a kind of Ng tube that has two balloons: a gastric and esophageal balloon. the gastric balloon is inflated first and is pulled firmly against the junction of the stomach and the esophagus using awaited traction which is usually created by a one-liter IV bag of saline.  this placement is confirmed, and the balloon helps to prevent migration of the tube into the airway.  the second balloon runs along the distal esophagus and is blown up to tamponade through esophagus.  the most important thing about this tube is that it needs to be secured properly to ensure it stays in the right spot. if migration upwards happens it can obstruct the patient’s airway.

 1 safety precaution to remember is to always have scissors at your bedside in case the balloon moves up and blocks the airway.

there are two other balloon tamponade tubes for GI bleeds called the Linton tube and the Minnesota tube they have similar characteristics to the SB tube

Treatment and prevention: Drug therapy

Scopic therapies or sometimes even with surgery depending on the severity we may be administering drugs to lower acidity or use vasoconstrictors that are only selective to the GI tract like vasopressin and more commonly octreotide as we mentioned earlier acid suppressive therapy is used to decrease acid content in the stomach in order to lower the risk for re bleeding: antacids which buffer stomach acid an increase gastric pH there is. histamine 2 antagonists like ranitidine an from oddity which lower volume and concentration of gastric secretions. most common drug in the setting of a GI bleed are PPI’s like pantoloc which directly block the release of gastric acids. for call that depending on the cause of the bleed treatment may vary. ulcers that are caused by H pylori would normally be prescribed a combination of both antibiotics and PPI's. Sulfracate is sometimes used with stress related ulcers to create a protective barrier on the surface of the gastric epithelium. it stimulates mucus and by cup secretion epithelial renewal and improves blood flow.

varices treatment is mainly aimed at decreasing portal hypertension so vasopressin an octreotide and sometimes even beta blockers are used for this reason you'll see that a lot of liver patients are on beta blockers.

 all critically ill patients should be considered to be at risk for stress ulcers. an GI hemorrhage patient at risk should be assessed for the presence of bright red or coffee grounds emesis bloody nasogastric aspirate bright red black or dark red stools any signs of bleeding should be promptly reported to the physician.

Module 3: Liver failure and Abd. Compartment Syndrome

Men body and as we mentioned in the review module it performs more than 500 defined functions. it is a primary processing facility of the body and is responsible for haematological function, detoxification, and storage bile, and bilirubin production, and nutrient metabolism.

 liver dysfunction can lead to a multitude of systemic problems whether it stems from the liver itself manifesting from a chronic or an acute disease or whether it's dysfunction is a result of another primary cause.

-       the blood supply of the liver: the hepatic artery carries oxygenated blood to the liver while the ported vein carries venous blood from the GI tract. The portal vein drains the majority of the blood from the GI tract, pancreas, and spleen and empties it into the liver. this circulation of nutrient rich blood between the GI tract and the liver is called portal circulation, where blood from the GI tract spleen and pancreas travels to the liver through the portal vein. the important of the portal circulation is that it allows harmful substances to be disposed of by the liver before moving into the vena cava and returning back to the heart. the portal circulation accounts for 75% of the liver's blood supply and even though it carries deoxygenated blood, it carries nutrient rich blood from the gut, pancreas, spleen, and stomach.

 The liver consists of four lobes. left, right caudate and quadrate. blood in the hepatic portal vein enters the liver by the underside of the organ along with the hepatic artery. a mixing of arterial blood from the lungs and nutrient rich blood from the gut, spleen, and pancreas pours into large endothelium line spaces called sinusoids that run between rows of hepatocytes, kupffer cells also line the sinusoids and these are specialized cells that are permanently situated in their walls which phagocytized Syria red blood cells, debrism and other foreign matter in the sinus blood. deoxygenated blood then drains into central veins and then out into the hepatic veins where it collects into the inferior vena cava

LOBULE AND PORTAL TRIAD

is hexagonal in shape. the liver cell parasites are organized into rows radiating from the central venue. the hepatic artery the hepatic portal vein and bile duct run parallel to each other and seem to sit at the circumference of this wheel this is often referred to as the portal triad mainly because of its triangular shape and its three major components hepatocytes also produced in secrete bile into special ducks called bile cuniculi which then drain into the branches of the bile duct to be concentrated and stored in the gallbladder.  this intricate network of vessels

liver function:

 liver the heaviest organ in your body and one of the most crucial this industrious structure simultaneously acts as a storehouse a manufacturing hub and a processing plant and each of these functions involves so many important sub tasks that without the liver our bodies would simply stopped working.

 one of the liver's main functions is to filter the bodies blood which it receives from two sources that hepatic artery delivers blood from the heart while the hepatic portal vein brings it from the intestine this double delivery fills the liver with nutrients that it then sorts processes and stores with the help of lobules. old blood flows also deliver the oxygen that the liver needs to function. the blood that is received from the intestine contains carbohydrates, fats, and vitamins, and other nutrients. in the case of carbohydrates the liver breaks them down and converts them into sugars for the body to use as energy.  when the filtered blood is sent back out sometimes the body has leftovers of nutrients that it doesn't immediately require, when that happens the liver hold some back stores it. when the body might need nutrients but the blood flowing into the liver isn't always full of good things it also contains toxins and by-products that the body can use and the liver monitors these strictly. when it spots toxic substance it either converts it into a product that can hurt the body or isolates it and whisks it away channeling it through the kidneys and intestine to be excluded.

transport fatty acids and help form blood clots to the cholesterol that helps the body create hormones. it also makes vitamin D and substances that help digestion.

liver uses cells called hepatocytes to convert toxic waste products into this bitter greenish liquid as it's produced and is into the gallbladder before being trickled into the intestine to help breakdown fats, destroy microbes, and neutralize extra stomach acid bile. also helps carry other toxins and by-products from the liver out of the body.

Liver disease:

potential problems that causes the liver to fail to perform its designated functions. the liver can be damaged in a variety of ways some examples include inflammation: while controlled inflammation is essential to maintain proper function an balance of the liver if it becomes dysregulated it drives the progression of liver disease called hepatitis

 obstruction of bile: bile flow can be restricted from blockages like gallstones, cysts, or tumors or, disease infection drug use, or genetic abnormalities. These can  cause bile to build up in the liver causing a liver disease known as cholestasis. accumulation of cholesterol: triglycerides abnormal retention of lipids within an organ is steatosis-> when it happens is often known as fatty liver disease. compromised blood flow to the liver can cause ischemia leading to inflammation and damage due to the inadequate oxygen supply being delivered an compromising liver function.

chemicals drugs minerals and infiltrates can damage liver tissues: as your liver is doing its job to process your blood I remove these toxins it can cause inflammation and damage to your liver if it goes on for awhile it can cause permanent damage as hepatocytes are injured and liver damage occurs.

 if there is an accumulation of fat deposits in the liver this is the beginning of fatty liver disease. this can lead to inflammation and fibrosis or scar tissue forms on the liver ->liver cirrhosis and cirrhosis is irreversible.

 liver disease and failure can be categorized based on the length of time the damage occurs over categories include acute, chronic, and acute on chronic acute liver disease: often caused by a viral or chemical happens suddenly and resolves becomes chronic or results in a patient's death liver failure ->having clinical manifestations within a period of 15 to 25 days an acute insult to the liver is also known as fulminant hepatic failure: which is a rapid deterioration of liver function in a person without prior liver disease this can result in widespread cell death and multi-organ dysfunction. it is defined by coagulation abnormality and hepatic encephalopathy occurring within two to six weeks of hepatic injury if the liver function does not return and liver transplantation is unavailable fulminant liver failure can progress to cerebral edema, coma, and death from brain herniation.

chronic liver disease leading to cirrhosis is typically more insidious in nature and is a slow deterioration that evolves over years disease processes affect the hepatocytes the blood vessels and the Kupfer cells which are responsible for uptake and subsequent degradation of foreign and potentially harmful substances in the body. if the injury is mild and reversible hepatocytes may regenerate and liver function may return to normal if the injury is more severe or sustained regeneration may be incomplete or the healing process may cause fibrosis.  fibrotic changes alter the liver and can lead to cirrhosis (an impediment of blood flow through the liver).

 acute on chronic liver failure occurs in patients who have underline advanced cirrhosis and experience. For example, secondary disease which causes acute liver decompensation.

risk factors for liver disease vary according to the type and cause of the disease what are the common underlying pathologies of liver disease that we see in the acute and critical care populations:

 cirrhosis is the end result of chronic ongoing liver disease when a substance or disease damages the liver necrosis of liver cells occur and scar tissue is formed this scar tissue is called fibrosis which progressively happens over the years when the entire liver has been scarred it hardens and shrinks in size and this damage is irreversible ->cirrhosis, usually caused from years of chronic injury.

 cirrhosis can be caused by alcoholic fatty liver, non-alcoholic fatty liver disease NAFLD and non alcoholic steelhead potatoes or Nash. NAFLD and Nash are common causes of chronic liver disease and are becoming more prevalent due to the increasing rates of obesity .

hepatitis: is inflammation of the liver in most cases due to a viral cause there are 5 unique hepatitis viruses identified by the letters ABCD&E while all of them caused liver disease they vary in important ways including modes of transmission, and vaccine availability.

Poisoning:  a leading cause of acute liver failure in the case of toxic drug overdose is acetaminophen overdose -> results in widespread hepatocyte damage and death leading to acute liver necrosis.

 Hypoperfusion and shock: for acute and critically I'll patients who experience shock or period of significant hypovolemic. hypotension profusion to the liver is impaired and this can result in damage to the liver.

Cirrhosis: liver it becomes thickened with heaps of protein an forms scar tissue so when your liver is constantly forced to process alcohol like or subject to a viral attack for a long time like in HBV or anything that causes a long-term or chronic state of liver cell or hepatocyte destruction and inflammation the liver could become seriously scarred and damaged to the point where it's no longer reversible-> fibrotic and in the liver ->. Cirrhosis. often referred to as end stage or late stage liver damage. when liver cells are injured they start to come together and form what are called regenerative nodules (classic signs of cirrhosis). with cirrhotic liver tissue you'll see that in between these clumps of cells or nodules is fibrotic tissue and collagen. these nodules which have fibrotic protein bands in between all right but how do these bands of fibrotic tissue form though. well fibrosis is a process mediated by these special cells called stellate cells that sit between the sinusoid and hepatocyte known as the para sinusoidal space.

 in healthy tissue these guys main function is to store vitamin A&R otherwise considered quiescent or sort of dormant when the hepatocytes are injured though they secrete paracrine factors that activate and sort of change this daylight cells when activated these stellate cells lose vitamin A proliferate and starts to creating transforming growth factor beta one or TGF beta which then causes them to produce collagen which is the main ingredient in extracellular matrix fibrosis and then scar tissue as this fire product issue builds up it starts to compress the central veins in sinusoids it's thought that in a healthy normal state these stellate cells play key roles in the natural wound healing process but when the liver cells are constantly injured the stellate cells are constantly activated and so they constantly produce collagen an factors that lead to fibrosis

Viral hepatitis: most commonly comes about because of a virus these viruses tend to target the cells in the liver and when they get in an infection, they tend to cause them to present these weird an abnormal proteins via their MHC. Class 1 molecules and at the same time you've also got these immune cells infiltrating the liver and trying to figure out what's going on and so the CD 8 positive T cells recognize these abnormal proteins as a sign that the cells are pretty much toast and the hepatocytes then go through site attacks to killing by the T cells and ptosis.  hepatocytes undergoing apoptosis are sometimes referred to as Councilman bodies this cytotoxic killing of the hepatocytes is the main mechanism behind inflammation of the liver and eventually liver damage in viral hepatitis. S&S fever malaise and nausea. additionally though patients might have hepatomegaly where their liver is abnormally large from inflammation which also might cause some pain and more damage is done to the liver, the amount of transaminase is in their blood will increase this is because your liver has these transaminase enzymes so it can do its job of breaking down various amino acids.  typically the serum amino transaminase or the amount in your blood is pretty low but when your hepatocytes start getting damaged they start leaking these into the blood so common sign is a greater amount of both alanine aminotransferase or ALt. and aspartate aminotransferase or AST typically even though both are elevated ALT will be greater than AST in viral hepatitis and will also be the last liver enzyme to return to normal.

 also elevated levels of atypical lymphocytes are common to see with viral hepatitis known as a typical lymphocytosis. hepatitis virus antigens patients often also end up developing jaundice with a mix of both conjugated bilirubin an unconjugated bilirubin. the conjugated bilirubin leaks out when bile duct are damaged or destroyed. when the hepatocytes die because those hepatocytes make up some of its lining. since these hepatocytes are dying you start to lose the ability to conjugate bilirubin and make it water soluble and so you end up with unconjugated bilirubin as well.  so since there's both conjugated and unconjugated bilirubin in the blood, some of the water soluble conjugated bilirubin gets filtered into the urine giving it this darker colour.  another common finding is increased urobilinogen in the urine urobilinogen is produced when bilirubin is reduced in the gut by intestinal microbes, most of that's reabsorbed and transported back to the liver to be converted into bilirubin or bile again but if these liver cells aren't working, t that irobilinogen is redirected to the kidneys so you end up with more euroball imagine in your urine.

 if symptoms continue or the virus sticks around for more than six months viral hepatitis goes from being acute to being chronic hepatitis at this point inflammation mostly happens in the portal tract and if inflammation and fibrosis keep happening we consider that a pretty bad sign since it might be progressing to post necrotic cirrhosis

Non alcoholic fatty liver disease: actually a spectrum of disease going from least to most severe steatosis. steatohepatitis fibrosis and finally cirrhosis. non-alcoholic fatty liver disease result from fat deposition in the liver which is unrelated to alcohol or viral causes.  typically it affects individuals with metabolic syndrome which includes: obesity, hypertension, diabetes, hypertriglyceridemia, and, hyperlipidemia . Although the exact mechanism of non alcoholic fatty liver disease isn't clear insulin resistance seems to play an important role. overtime insulin receptors on various tissues including the liver becomes less responsive to insulin and as a result the liver goes into a mode where it increases fat storage and decreases fatty acid oxidation. decrease secretion of lipids into the bloodstream in the form of lipoproteins and increase synthesis and uptake of free fatty acids from the blood a process called steatosis. steatosis -> cause the hepatocytes to swell up with fat and push the nuclei to the edge of the cell. that fat in the hepatocytes becomes vulnerable to degradation. the process of steatosis, an inflammation is referred to as Steatohepatitis in the absence of alcohol this is called non alcoholic steatohepatitis or Nash. in addition to bloating and dying hepatocytes there might be additional histopathologic changes like the presence of Mallory denk bodies which are tangles of intermediate filaments that can be seen in the cytoplasm of parasites the mechanism though for how these form is still unclear about a side damage also attracts neutrophils into the liver tissues and finally chronic steatohepatitis can cause liver stellate cells to lay down by-product issue causing the disease would be classified as fibrosis as the process of fibrosis continues the overall architecture of the liver changes to the point where the disease is classified as cirrhosis

Clinical representation of liver failure

Presentation of liver failure here you can see the signs and symptoms of liver cirrhosis as well as physical findings associated with liver failure

edema and ascites: when liver damage progresses to an advanced stage fluid accumulates in the legs and the abdomen

bruising and bleeding: when the liver slows or stops producing proteins required for clotting a patient with liver disease will bruise or bleed more easily hepatomegaly or the liver becomes enlarged

 jaundice: when the disease liver does not remove enough bilirubin from the blood it turns the skin and white of the eyes a yellowish colour and the urine can become very dark in colour

hepatic encephalopathy and liver failure:  the liver cannot clear toxins from the blood these toxins accumulate in the brain causing decreased mental functioning including confusion, personality changes, memory loss, inability to concentrate change, in sleeping habits and can even cause coma as liver failure progresse patients will likely also exhibit weakness and fatigue loss of appetite abdominal pain and bloating from the accumulation of ascites

 itchy skin and spider like blood vessels on their skin called spider angioma

Hepatic encephalopathy :

results from the buildup of ammonia in the blood it can cause a wide spectrum of neurological abnormalities and if it is not managed. can result in cerebral edema and increased intracranial pressure. this chart provides a clinical assessment guide which focuses on level of consciousness, orientation, intellectual function, behavior mood, and neuromuscular function depending on the severity of the encephalopathy. patients can present in different ways you can see patients that are awake and very restless or agitated or the polar opposite of the spectrum where patients can be stimulant or even comatose these are important to know, as knowing the early indicators of hepatic encephalopathy can aid in early detection and treatment.

 treatment for hepatic encephalopathy involves cleansing the bowels using Lactulose.  Lactulose binds to the ammonia and is then excreted which helps to clear the ceremonial levels.  Lactulose is the primary intervention given to patients with hepatic encephalopathy patients may also have their dietary protein intake decreased as well or can be given antibiotics to aid in management up the encephalopathy

liver failure treatment and management

prevent progression of the liver damage if possible management will also be directed as supporting the cardiopulmonary status.  haematological and nutritional functions and preventing and treating complications this takes an interprofessional approach.

supporting cardiopulmonary status includes:

 monitoring of fluid balance which is important for the nursing management in support of a liver failure patient. some patients may have a fluid volume deficit due to complications of bleeding, coagulant abnormalities, an ascites. or patients may be volume overloaded because of having low albumin levels and sodium excess if patients are volume overloaded the healthcare team may consider diuretics like sparolactone or furosemide.

 paracentesis may also be required to relieve the ascites or painful tightness felt in the abdomen

monitoring respiratory status and oxygenation in order to maintain adequate gas exchange you must be mindful of the use of sedatives and analgesics and you want to keep the head of the bed elevated to improve breathing

hematologic nutritional and metabolic functions:

monitor for signs of bleeding, , bruising, and petechiae and report new findings to your healthcare team. administration of blood products may be required initiate oral nutrition and supplement action protecting patient from injury and treating complications.

provide comfort and emotional support to these patients you want to diligent skin assessment and reposition patients to decrease skin breakdown or injury

limit the use of medications like sedatives and analgesics that are metabolised in the liver as they will cause further damage and will accumulate in the patient closely observe for changes in mental status which could include hepatic encephalopathy or worsening hepatic encephalopathy due to cerebral edema report any changes to the healthcare team an advocate for appropriate treatment to reduce ammonia levels.

 hepatorenal syndrome is a form of renal failure caused by liver disease aggressive diuresis or elevated systolic blood pressure. can cause acute renal dysfunction so carefully monitor for changes in renal function. prepare the patient for potential liver transplantation. liver transplantation will be considered when complications cannot be controlled or treated

Abdominal compartment Syndrome:

Intra abdominal pressure:

 the pressure within the abdominal cavity. there is only so much stretch available. when pressure within the abdominal cavity rises such as in the cases of bleeding, sepsis, peritonitis, and even liver failure.  normal intrabdominal pressure is less than 7mm of mercury and critically ill adults normal is between 5 and 7mmHG above this is considered increased and can have detrimental effects on organ systems both within the abdominal cavity an outside it as well.

 intra abdominal pressure is measured via bladder pressures where a transducer is attached to the patients Foley catheter and attached to a monitor to obtain a pressure reading.

so in normal conditions there is a normal intraabdominal pressure which is below 7mmHg, when pressure increases from normal intraabdominal pressure then you get into abdominal hypertension an if the pressure continues to increase that it results an abdominal compartment syndrome

         normal IAP, if pressure increases then it leads to intra-abdominal hypertension, if that pressure increases then it leads to abdominal compartment syndrome.

Effect of IAH 12-15 mmHg:

when the intra abdominal pressure is between 12 and 15mmHg,the impact of this increased pressure can be noted as pressure increases there is increased compression of vessels and increase systemic vascular resistance as the vena cava is compressed, preload will be decreased. In turn due to decreased preload cardiac output will also be decreased, breathing will also become difficult as pressure increases because the pressure pushes against diaphragm. if your patient is mechanically ventilated there will be increased peak pressures noted on the ventilator as it will take more pressure to push the air into the lungs.  within the abdomen itself there will be decreased perfusion to the organs leading to increased organ ischemia especially of the intestines

 as the pressure increases to 16 to 20mm of mercury:  these symptoms will worsen. the worsening vena cava compression further decreases cardiac output and there will be a falsely elevated CVP and wedge pressure. as now the pressure within the abdomen is pushing on the thoracic cavity increasing the pressure within it as well this will also result in increased lung dysfunction as this will increase intracranial pressure there will be a decrease cerebral perfusion. pressure and changes to the patient's neurological status such as decreased level of consciousness may be noted there is increased bowel edema an ischemia as profusion continues to be compromised and the decrease perfusion to the kidneys will result in an acute kidney injury and in turn cause a metabolic acidosis

 once the pressure exceeds 20mm of mercury: this becomes a very serious situation of abdominal compartment syndrome the vena cava is now flattened and between decrease venous return and increased intrathoracic pressures there will be cardiovascular instability, the brain swelling, and ischaemia will result in a very decreased level of consciousness ,or even coma. the gut will now be ischemic and necrosis is impending metabolic acidosis will worsen .

 there are three main cardinal signs of worsening abdominal compartment syndrome:

-       abdominal distention

-       the patient is having difficulty breathing or there's elevated peak pressures on the ventilator

-       decreased urine output.

these should all trigger you that abdominal compartment syndrome is worsening. other clinical signs include: mental confusion, worsening hypoxemia, hypotension, tachycardia, and jugular venous distension.

 nursing consideration:

 turning off enteral feeds, and discussing with the team the continuation of enteral feeds or having a discussion with the team and doing an assessment for the insertion of an Ng tube or rectal tube for decompression

 call the RT to perhaps lower the peep change tidal volumes as directed in order to decrease intrathoracic pressure and in turn decrease intra abdominal pressure.

in order to improve abdominal wall compliance: regularly assess pain status and ensure adequate pain control and sedation .positioning patients in reverse trendelenburg if possible.

 in order to relieve abdominal pressure be mindful of the amount of fluids going into the patient and avoid a positive cumulative balance. antiemetics may be required to prevent vomiting and retching which can cause increased intracranial pressure and be prepared to assist the physician in any interventions to evacuate space occupying fluid like inserting a drain at the bedside ultimately the definitive treatment for abdominal compartment syndrome and organ dysfunction where initial treatments have been unsuccessful is surgical decompression this will usually happen in the OR so you may have to prepare your patient for that.

MODULE 4: PACREAS

pancreas is a gland that sits directly behind the stomach.

its exocrine function is to release digestive enzymes to help breakdown proteins, carbohydrates, and fats. anatomically it's made-up of the head, the body, and the tail. the main pancreatic duct runs along the entire length of the pancreas eichel exes digestive enzymes from each lobule and dumps it into the ampulla Vader: a convenient meeting point where the common bile duct joins with the main pancreatic duct at the entrance to the duodenum-> dumping both bile and pancreatic juices to aid in the digestion of food.

 Exocrine function: the pancreas has two functions approximately 99% of the function of the pancreas is to produce pancreatic juice made-up of water sodium, bicarbonate, and digestive enzymes.

the remaining 1 to 2% of its function is its endocrine role which mainly involves regulation of blood glucose levels.

 the term exocrine refers to the release of a substance outside the body, whereas the term endocrine refers to the release of a substance into the blood. So the main exocrine function of the pancreas: is to breakdown or digest components of food into nutrients that can be absorbed and used by the body when food leaves the stomach and enters the duodenum, it signals the sphincter at the ampula Vader to relax and allow the release of pancreatic juice into the duodenum at which point it mixes with bile pancreatic juice, consists mainly of water and sodium bicarbonate. the purpose of the sodium bicarbonate is to decrease the acidity of the kind as it passes from the stomach into the duodenum but the pancreatic juice also consists of enzymes that are essential in the digestion of starch, protein, and fats. there are three main enzymes: amalyse-> that breaks down carbohydrates or starches into glucose. Proteases-> that breakdown protein into amino acids and lipases-> that breakdown fats into fatty acids an monoglycerides.

 The enzymes need to be activated to do their jobs. They become active within the duodenum(enzymes become activated bile from the gallbladder enters the duodenum at the major papilla from the common bile duct).

it breaks apart fat into smaller fat droplets which then become easier for Lipase to digest the release of regulation of pancreatic enzymes. The enzymes are able to respond to signals from the intestinal hormones secretan and cholecystokinin which stimulate the pancreas to secrete the pancreatic juice

from the cellular level exocrine function of the pancreas is served by its acinar cells centre. acinar cells and interpolated ducks acinar cells make and secrete digestive enzymes. these cells are found in the pancreas and they are grouped together. duck cells which align the walls secrete the bicarbonate solution to help protect and neutralize the city of the kind. within the acinar cells are little granules called cimage and granules zymogen granules are like little bubbles in the cell that keeps zymogen safe from proteases the terms daimajin is given to an enzyme that isn't functioning yet that is an inactivated enzyme because it's still surrounded by a protective layer these protective layers act like rappers this rapper is a metaphor for the link that exists between two amino acids and so these enzymes in their inactivated form become activated when proteins is cut or break the bond between these amino acids sometimes they can even become activated on their own

So what if a patient's pancreas produces too many enzymes or one of the pancreatic ducts are blocked (gallstone) or what if for some inexplicable reason these enzymes get activated before they reach the duodenum?

well if these enzymes are activated before reaching the duodenum, pancreatitis can occur pancreatitis: is a condition in which the pancreas becomes inflamed as a result of activated enzymes causing pancreatic damage. pancreatitis can be acute or chronic. the acute form occurs suddenly and can be very severe and lead to death. chronic pancreatitis occurs when there is continuous damage to the pancreas that can lead to ongoing pain and a permanent decrease in its function.

acute pancreatitis: is the sudden inflammation in hemorrhaging of the pancreas due to destruction by its own digestive enzymes ->auto digestion. most of the time the disease is actually relatively mild but it can easily become severe so it's critical to diagnose and treat it quickly.

 the pancreas is a long skinny gland the length of a dollar bill and is located in the upper abdomen or the epigastric region behind the stomach.

 it plays endocrine roles for example alpha and beta cells make hormones like insulin and Glucagon that are secreted into the bloodstream but it also plays exocrine role for example acinar cells make digestive enzymes that are secreted into the duodenum to help digest food.

 these pancreatic digestive enzymes breakdown macromolecules like carbohydrates lipids and proteins found in food. but these macromolecules are also found in the cells of the pancreas to protect the pancreas. the acinar cells manufacture inactive forms to the enzymes called proenzymes or zymogens. these enzymes are normally activated by proteases which cleave off a polypeptide chain. for additional security the zymogens are kept away from sensitive tissues in storage vesicles called zymogen granules and are packaged with protease inhibitors that prevent enzymes from doing damage.  if they become prematurely active to digest,  these enzymes are released into the pancreatic duct and delivered to the small intestine, where they are activated by the protease trypsin to the pancreatic digestive enzyme that's produced as the zymogen trypsinogen .

if trypsinogen and the zymogens become activated too early then it can cause acute pancreatitis and this might happen as a result of any injury to the acinar cells or anything that prevents the normal secretion of the proenzymes into the duodenum.

the two leading causes of acute pancreatitis are: alcohol abuse and gallstones alcohol abuse: alcohol increases zymogen secretion from acinar cells while decreasing fluid and bicarbonate production from the ductal epithelial cells. as a result the pancreatic juices become really thick and viscous potentially forming a plug that can block the duct. pancreatic juices start backing up increasing the pressure an leading to distension of the duct itself at the cellular level.

consequence of this is that membrane trafficking becomes chaotic simonton granules might fuse with lysis ohms which brings trypsinogen into contact with lysosomal digestive enzymes. trypsinogen might then be turned into activated trypsin which begins the cascade of digestive enzyme activation and auto digestion of the pancreas. alcohol also contributes to pancreatitis in other ways though for example stimulating acinar cells to release inflammatory cytokines which attracts a strong immune reaction.  neutrophils arrive quickly to the scene and often really super oxide and other proteases which contribute to the problem finally it's thought that high consumption and subsequent oxidative metabolism of alcohol might produce enough reactive oxygen species to overwhelm cellular defences in damage to cells.

  Gallstones: sometimes get lodged in this sphincter of ODI which blocks the release of pancreatic juices which is pretty similar to the alcohol induced protein plug. so in acute pancreatitis there's pancreatic tissue destruction that results from the protease. this can cause tiny blood vessels to become leaky and sometimes rupture ultimately all this extra fluid causes swelling and unfortunately there could be some activation of Lypase. was going to destroy the fat around the pancreas or para pancreatic fat all of this digestion and bleeding can actually liquefy the pancreatic tissue a process called liquefactive hemorrhagic necrosis.

in addition to destroying the pancreas, pancreatitis can cause serious complications like the formation of a pancreatic pseudocyst: forms within fibrous tissue surrounds the liquefactive necrotic tissue of the pancreas and this fibrous tissue develops a cavity that fills up with pancreatic juice.

 abdominal pain ,loss of appetite, and a palpable tender mass which follows a bout of acute pancreatitis are suggestive of a pancreatic pseudo cyst in addition serum amylase lypase and bilirubin might sometimes be elevated

an abdominal CT scans the best way to image a pancreatic pseudocyst since they swell in size. pancreatic pseudocysts have the potential to rupture which causes hemorrhage and release of pancreatic enzymes into the abdominal cavity which will lead to a massive inflammatory reaction that pseudo cyst can also get infected often by E coli and turn into a very dangerous pancreatic Abscess. this presents similarly to a pseudo sis but with the hallmarks of an infection including a high fever and high white blood cell count

Physiology:

pancreatic duct be that due to gallstones thickening mucus or even a tumor which results in the activation of the pancreatic enzymes while they're still in the pancreas can cause auto digestion ->  triggers an inflammatory process which increases permeability and allows fluids to shift into the interstitial space causing edema and because the pancreas is such a vascularised organ hemorrhage can ensue and because it's also a fatty organ, fat necrosis may happen

acute pancreatitis is categorized into two types interstitial oedematous pancreatitis or necrotizing pancreatitis the extent of injury determines what type of acute pancreatitis.

Interstitial Edematous: inflammatory cells and interstitial edema are present within the parenchyma but the acinar cells structurally appear intact and blood flow maintained through the small vessels

Necrotizing: if the injury to the cells is severe and cellular destruction has occured in the pancreas. often associated with hemorrhaging (hemorrhagic necrotizing)

pancreatitis is characterized by considerable necrosis hemorrhage of the tissue vascular inflammation. thrombosis and fat necrosis acute pancreatitis can also be classified as mild moderate or severe based on physiological findings lab results and imaging severe acute pancreatitis or SAP is associated with prolonged ICU stay and a higher mortality rate but if the cause is identified and removed or treated promptly recovery can be expected

 the major causes associated with acute pancreatitis:gallstones, alcohol, and trauma.

 gallstones account for approximately 45% of cases and are the most common cause of pancreatitis. the pathogenesis of pancreatitis related to gallstones is relatively unknown, however many believe that the obstruction of the major papilla by the gallstone causes a reflux of bile into the pancreatic duct

 alcohol is the second leading cause of pancreatitis and accounts for approximately 35% of cases alcohol causes pancreatitis through a variety of mechanisms including having toxic and metabolic effects on the pancreas.

obstructions of the smaller ducts from protein plugs and causing abnormal sphincter of oddi motility there are many other potential causes as well the chart on your screen covers the other potential causes of acute pancreatitis sometimes the cause is unknown in which case is termed idiopathic this accounts for approximately 10% of the cases

Clinical representations:

Abdominal pain: be localized to the left upper quadrant mid epigastric area with possible radiation to the spine/flank/back and shoulder. it is often exacerbated when the patient lies supine but patients can get some relief from the tripod position.  pain usually begins abruptly after a large meal or large intake of alcohol. pain also tends to be accompanied by nausea and vomiting. patients will tend to be tachycardia and maybe hypotensive due to fluid losses an shifts other common clinical presentations include Cullen sign (umbilicus brusing) and grey Turner( flank/side bruising) which is indicative of retroperitoneal bleeding.  these happen as necrosis induced hemorrhaging spreads to the soft tissues of those body areas

Persistent abdominal pain diagnostic testing

when acute pancreatitis enzymes are released into the bloodstream serum blood work will indicate elevated levels of these enzymes the most common enzymes are amalyse, lipase. these elevated levels are both indicative of pancreatitis. abnormal presence in the blood indicates damage to pancreatic cells. Lypase is more specific or reflective of acute pancreatitis however amalies elevations are more sensitive because amalies is present in other body tissues and other disorders may contribute to an elevated level.  

an elevated white blood cell count could be present due to infection and a low hemoglobin level due to hemorrhage.

one significant change you will see in the presence of tissue necrosis is hypocalcemia this is because calcium binds with fatty acids during tissue necrosis also trypsin inactivates parathyroid hormone which is needed for calcium absorption

other findings like hyperbilirubinemia elevated bilirubin and elevated liver enzymes could be related to a retained stone in the bile duct or compression of the bile duct.

diagnosis CT scan is the imaging method of choice in delineating the pancreas as well in determining the severity and complications for this reason it is considered to be the gold standard. Shows: nectosis, inflammation and pseudocyst

 Ultrasound may show Gallstones.

Ranson’s criteria

Tool used to determine severity and mortality of pancreatitis.  if the patient has zero to two factors present the predicted mortality is 1%

three to four factors 15% mortality

 five to six factors 40% mortality and

seven or more factors predicted mortality rate is 100% in essence this shows that his pancreatitis progresses mortality exponentially increases as well

Complications:

With acute pancreatitis other complications of acute pancreatitis include:

 serious internal bleeding or hemorrhage from a damaged blood vessel which can quickly develop into hypovolemic shock

systemic activation of blood coagulation factors or disseminated intravascular coagulations or DIC: tiny blood clots start to develop throughout the body using up all of the clotting factors which paradoxically make it easier to bleed as well basically upsetting the balance of clotting homeostasis and potentially damaging various vital organs

acute respiratory distress syndrome: which is where massive pancreatic inflammation leads to leaky blood vessels throughout the body which makes it hard to breathe ARDS is the leading cause of death among people with acute pancreatitis

Consequences: look at the ppt.

Nursing Management:

Thus providing supportive care immediately which includes fluid and electrolyte replacement, nutritional support, and attentive pain management.

monitor for systemic and local complications let's review some components of supportive care and treatment pain management acute pain is a universal sign of acute pancreatitis and treatment of pain is a top priority because pain can increase exocrine enzyme release which worsens inflammation and hemodynamic instability. the use of a reliable pain rating scale is necessary in order to assess pain and then administer analgesics as prescribed if possible position the patient in a knee to chest position this can help to alleviate the intensity of the pain.  fluid and electrolyte replacement pancreatitis is associated with massive fluid shifts resulting in 3rd space losses vomiting and vascular permeability related to inflammatory mediators hypovolemia in a patient with pancreatitis is dangerous as it can compromise pancreatic perfusion and exacerbate pancreatic necrosis. intravenous crystalloids Ann coy Lloyds are administered immediately to prevent hypovolemic shock and maintain hemodynamic stability you want to monitor closely for cullen sign an grey Turner sign which indicate bleeding in the peritoneum. electrolytes are monitored closely an ensure that abnormalities such as hypocalcemia, hypokalemia, and hypomagnesemia are corrected. hyperglycemia may also be present due to the stress response and impaired insulin secretion ministration of IV insulin may be required providing nutritional support and correcting metabolic alterations. enteral feeding is safe and cost effective and that it is associated with fewer septic and metabolic complications than any other methods. it enhances immune modulation and maintenance of the intestinal barrier and avoids complications associated with parental nutrition like infection enteral feeding can be considered within that first 24 to 48 hours PPN can still be considered for critically ill patients if they cannot tolerate enteral feeding but enteral feeding is preferred administration of medications to block the secretion of pancreatic enzymes or facilitate nutrient absorption may also be given intensive monitoring of each organ system is imperative because organ failure is a major indicator of the severity of the disease because progression can lead to hypovolemic shock RDS acute kidney injury and GI hemorrhage hypovolemic shock as a result of relative hypovolemia can be caused by the release of widespread inflammatory immune mediators which can then affect other organ functions necrotic areas of the pancreas can lead to development of a widespread pancreatic infection which then can also lead to systemic infection an increases the risk of death when it comes to antibiotics it should not be used prophylactically but only in the presence of sepsis Abscess and biliary calculi if a patient develops infected necrosis surgical debridement is necessary the procedure is the minimally invasive necrosectomy and it entails careful debridement of the necrotic tissue in and around the pancreas is the patient has a pancreatic pseudo cyst this is a collection of pancreatic fluid enclosed by a non epithelialized wall it can resolve spontaneously rupture which results in hemorrhage become infected resulting in Abscess or invade surrounding structures resulting in obstruction treatment is drainage of the pseudo cyst surgically and endoscopic or percutaneously

MODULE 5: BOWEL OBSTRUCTION

Theres a mechanical or a functional impairment of the intestines which prevent the normal movement of digestive products through the intestinal lumen this results in a build-up of ingested fluid or food along with digestive secretions within the intestinal lumen above the obstruction. this buildup becomes an issue because the bacteria found in the gut wall continues to grow when exposed to food and produces gas.

obstructions can be classified as either partial or complete depending on the degree of obstruction and can occur in the small or large bowel. prompt recognition of a bowel obstruction is imperative for the nurse because an intestinal obstruction can progress to bowel strangulation which can have life threatening complications such as bowel ischemia/infarction perforation or sepsis.

bowel obstructions occur because of mechanical obstruction or a functional impairment, mechanical obstructions can be due to intrinsic or extrinsic factors. intrinsic factors cause a blockage of the internal lumen of the intestine whereas extrinsic factors are caused by something that compresses about illumine from the outside of the intestine.

 the five main causes or types of mechanical obstruction are adhesion's tumors intussusception hernia and volvulus.

 functional obstructions do not have a physical blockage present however there is still no movement through the digestive tract functional obstructions are commonly categorized as an ilius or colonic pseudo-obstruction which is also known as Ogilvie syndrome.

 there are five types of mechanical obstructions click on each image to learn more

types of mechanical obstruction

Abdominal Herniation: an organ pushes through an opening in the muscle or tissue that holds it in such as in the case when part of the intestine bulges through the abdominal wall hernias carry a high risk of complete obstruction and strangulation

Adhesion: fibrous tissues within the abdomen those causing bowel obstructions may form bridges between segments of the bowel be that within the lumen of the bowel or if it forms around loops of the bowel. adhesions are the most common cause of bowel obstruction in the small intestines the most common development of adhesion's is following abdominal surgery they can also develop after abdominal radiation ischaemia infection or as a result of foreign bodies in majority of individuals adhesions do not cause any issues however in some individuals adhesions may block the intestines so that an obstruction occurs the more dangerous situation is when a loop of bowel maybe entrapped by fibrous bands so the bowel becomes obstructed at two points along its course forming a closed loop these patients have a high risk of ischemia due to venous infarction which can cause perforation and subsequent septic shock

Volvulus: caused by Loop in the intestines set twists around itself the term volvulus comes from the Latin word volvere which means to roll and so the intestines twist around itself and its surrounding mesentery the three most common types of volvulus are sigmoid volvulus, cecal volvulus, and midgut volvulus

Intussusception: part of the intestine folds in on itself causing an obstruction this is less common in adults but is the most common cause of intestinal obstruction in infants and small children intussusception usually occurs around the ileocecal region of the intestines this is where the ileum of the small intestines and the cecum of the large intestines meet almost all of intussusceptions occur when the ilium folds into the cecum.

Tumor: when the growth extends into intestinal lumen and blocks passage adenocarcinoma of the colon and ****** is the most common tumor obstruction most common in individuals over 60 years of age as you can see in the diagram colorectal cancer can occur anywhere in the colon and is increasingly more common which is why screening via endoscopy is important in catching abnormal growth early called polyps.

Functional Obstruction:

Intestinal contents to pass through the intestinal lumen this can be due to either myopathy, neuropathy, or a combination of both. for example muscle or nerve problems will disrupt the normal coordinated. muscle contractions of the intestines slowing or stopping the movement of food and fluid through the digestive system, thereby causing a functional obstruction although the exact pathophysiology is poorly understood, in an ileus peristalsis ceases and extension of the intestine occurs and there is no movement of bowel contents through the intestines it can occur in both a small bowel and the colon .

common causes of an ileus include: drugs like opioids, electrolyte abnormalities, ischaemia, neurogenic causes, infection, metabolic abnormalities, and abdominal surgery. Ogilvie pseudo obstruction occurs without a definable mechanical cause and usually results in acute mark distention of the colon often just limited to the colon and not the small bowel which differentiates it from an alias which can include both as you can see in the image there is an extreme distention of all segments of the colon due to the buildup of gas it can be a chronic condition of recurrent distention of the colon an is usually diagnosed after excluding mechanical lower bowel obstruction commonly it occurs in hospitalised.  older adults people with neurological disease, trauma patients, or surgical patients with underlying disorders. ileus obstructions can occur in the small or large bowel and can be classified as either partial or complete depending on the degree of obstruction the most common cause of large bowel obstruction are tumors causing approximately 90% of obstructions in approximately 50 to 70% of all cases of small bowel obstructions adhesions are the result often related to prior abdominal surgery hernias and tumors are also common causes of small bowel obstruction as well the cascade of events as a result of a bowel obstruction are very similar in a bowel obstruction of the small or large intestines regardless of whether it is a mechanical obstruction or functional obstruction we will review the slight difference of clinical presentation in later discussions

obstruction means that the material the substance that we eat cannot pass through our bowel smoothly it accumulates in the area and this can result in a few. so food that pileups here can be metabolise by the bacteria that are normally residing in the area to produce gas. gas accumulates causing a bowel distension which can compress the vessels that supply the bowels. so we can have venous compression this means that we have decrease in oxygen supply to the area to the bowel and thus we have decrease in oxygenation. decrease in oxygenation results in a few things:

 the cells of the intestine die

second no oxygen supply decreases peristalsis further aggravating the bowel distension. more distention decrease in oxygenation also promotes the bacteria in the area to enter circulation because their anaerobic. all these are these are toxins that can enter the circulation resulting in some form of sepsis.

when we breathe air goes down our intestine is normal but this realistically aggravates the bowel, essential it promotes the distention of the bowel.  so  compresses the vessels we get venous compression and when we have venous compression, can actually result in fluid piling up in this area it just gets to carry it out into the bowel. when fluid is being secreted into the bowel we lose water and when we lose water we lose electrolytes an when we lose electrolytes and water this results in hypotension => shock.

so bowel distention simply results in hypertension also when we get distention of the bowel, this triggers some nerves in the valve which sends signals up to the brain to trigger the vomiting response because the brain thinks that there's something wrong in this area and it wants to get rid of it so vomiting is triggered but vomiting doesn't really help because when we vomit we lose water and we also lose electrolytes which results in hypertension again so we get hypovolemic shock so shock can result from hypotension or shock can result from sepsis which is when we get you know the bacteria entering the circulation

Complications:

Bowel obstruction there are 4 main complications ischemia, perforation, sepsis, and shock.

 when this tension due to the buildup of gas and fluid causes venous compression healthy bowel does not get enough oxygen supply resulting in ischemia and ultimately cell death necrosis results in toxin release into circulation as well it allows for bacteria to move from the bowel into circulation. if the bowel is extended too much due to the gas and fluid build-up beyond a certain point, it will perforate releasing contents into the peritoneum this can cause massive problems including peritonitis. if the bowel distention is not relieved and the pressure within the bowel causes it to perforate this will release bowel contents into the peritoneum which can result in peritonitis and sepsis can also occur as a result of the systemic dissemination of toxins and bacteria associated with tissue ischemia dissension begins almost immediately as gases and fluids accumulate proximal to the obstruction. dissention increases the secretion of fluids within the intestine however the ability of the intestines to reabsorb water and electrolytes into the lumen is compromised this results in severe fluid and electrolyte disturbances and the third spacing of fluids results in dehydration and hypovolemia -> hypotension -> hypovolemic shock. the patients’ vital signs are likely to indicate hypovolemic shock there may be early subtle signs such as a raised respiratory rate, the temperature may also be slightly raised due to the inflammatory process.

 symptoms of distention nausea and vomiting and pain and should be closely watched for signs and symptoms of the complications of sepsis, perforation, ischemia, necrosis.

 this chart provides a summary of the most common clinical presentations of bowel obstructions so pain, vomiting, abdominal distention ,and Constipation. however different variations of these symptoms will be based on the location of the obstruction. for small bowel obstructions, pain is more severe and more proximal to the obstruction abdominal cramps around the umbilicus or in the epigastrium tends to be intermittent however severe steady pain suggests that strangulation has occurred. vomiting is common with obstructions higher up in the small bowel and the vomit will consist mainly abilius content. patients with partial obstruction may develop diarrhea.

 Constipation is a late sign for large bowel obstruction symptoms are usually a bit milder and develop more gradually. pain is variable often milder in comparison with the pain associated with a small bowel obstruction. if there is vomiting it maybe feculent nature and this is considered a late sign of an obstruction in the large bowel the key features however are distension in large bowel obstructions and also Constipation because of the variation in clinical presentation a thorough clinical assessment provides valuable information both for early identification of issues bark and provide information to guide the formulation of a plan of care for the patient the order of steps in the focus abdominal assessment are altered slightly to prevent stimulation of GI activity.

 therefore, the order followed should be to inspect first followed by auscultation then percussion and finally palpation.

 the abdomen can be divided into 4 quadrants or 9 regions with the umbilicus  

clinical assessment of a patient with a bowel obstruction an

1)  inspection of the abdomen dissension maybe obvious especially in situations of a large bowel obstruction peristalsis should not be visible alisa patient is very thin if increased peristalsis is observed this can be an indication of an early obstruction scars may suggest possible adhesions as the cause of a small bowel obstruction.

2) auscultation focuses on two things: evaluating bowel sounds and assessing for breweries in obstruction abnormalities and bowel sounds can be found normal bowel sounds include high pitched gurgling sounds occurring every 5 to 15 seconds and approximately 5 to 30 * a minute in the large intestine that sounds more lower pitched and more of a rumbling quality. one of the main early signs of obstruction is hyperactive bowel sounds these sounds are high pitched tinkling with peristaltic rushes coinciding with cramps this is because the gut initially tries to push the contents along to increase peristalsis but once the mechanisms start to kick in peristalsis slows down and stops decreased or hypoactive bowel sounds are associated with late bowel obstructions sounds are infrequent and abnormally faint however when there are no bowel sounds auscultated in a 5 minute. This is then a situation of absent bowel sounds which may be a sign of bowel ischaemia

 3) percussion of the abdomen includes tympani or hyperresidents over the intestine however increased tympany maybe found due to gaseous distention.

4) with infarction the abdomen becomes tender therefore palpation is likely to illicit tenderness and guarding in this case. palpation may also reveal mass of striangulated hernia and sometimes dilated loops of bowel can be palpable.

 if a bowel obstruction is suspected the priority treatment is to address the underlying cause in order to do this

the first goal of care:

 is to identify the level and source of the obstruction X-rays can be done to confirm the diagnosis of complete obstruction and sometimes is able to help with localising the site of obstruction as multiple airfield levels may be visible with a step ladder pattern that demonstrates multiple loops of dilated bowel with different air levels but CT scans can provide more information regarding the specific site of obstruction by showing the entire abdomen and being able to identify any other complications such as strangulation. CT scans can determine the difference between a mechanical obstruction versus a functional obstruction like an alias as well they can pick up any complications of an ileus  therefore CT scans are the diagnostic examination of choice

 the second goal of care is pain management for this analgesics may be ordered and administered be mindful to avoid excessive use of opioids which can delay the return of peristalsis. if analgesia is provided this will likely be done in conjunction with treatment of the cause of the pain which brings us to our third goal of care.

 the third goal of care is decompressing and emptying of the GI contents. to relieve dissension and nausea the management of bowel obstructions is centred around decompression of the GI system by an insertion of an NG tube which the physician will order to have attached to either straight drainage or intermittent suction on a low setting often ordered as low gomco. as many institutions have transitioned to wall section setups low gomco is considered less than 90mmHG on the wall units.  you can check the level of suction by occluding the tubing while suction is on remember when it is in the intermittent mode wait for approximately 20 seconds for the section to begin for lower obstructions the colon may be decompressed via rectal tube or colonoscopy procedure. antiemetics may also be ordered and administered to help manage nausea and vomiting

 continuous assessment of the patient is very important to determine whether the obstruction is resolving or worsening as well as it helps to monitor the patients fluid and electrolyte status with the obstruction water and electrolytes will accumulate in the lumen of the intestine leading to dehydration and hypovolemia electrolyte imbalances also occur with hypochloremia hypokalemia and metabolic alkalosis being the most common abnormalities especially if the patient is vomiting or has large losses from their Ng tube.

 4^th: the restoration of the patient's fluid and electrolyte balance administration of crystalloid or colloid fluid to treat fluid volume deficit is necessary instant outs need to be closely monitored in patients with bowel obstructions as this will help to assess the patients response to fluid resuscitation and their risk of dehydration gastric output should be included in this and followed closely as replacement fluid may be ordered by the team blood work is important to regularly assess because it helps to direct the management of bowel obstructions electrolyte imbalances hemoglobin hematocrit and white blood cell counts are followed closely in order to assess whether the patient is experiencing dehydration progressing to hypovolemic shock or progressing to sepsis electrolytes should be replaced as per orders

Some additional considerations that you should make is that as the abdomen continues to be distended it can impair respiratory function remember to elevate the head of the bed no greater than 30 to 45° or if possible use reverse trendelenburg to minimize abdominal compression from the flexion of the hips assist the patient with deep breathing and coffee and exercises to expand lungs and to mobilize secretions. provide nutrition via enteral feeding as ordered early enteral feeding as slow rates may be considered as it can assist the return of peristalsis if all ischemia is suspected or if the patient is suspected to be NPO for an extended period of time then TPN may be considered. if patients begin to pass gas and stool supportive management is continued but if patients show no improvement within 24 to 48 hours or if a fever and or rebound tenderness occurs the administration of broad spectrum antibiotics is initiated and surgical evaluation is indicated immediately some surgeries associated with obstructions include license of adhesion's reduction of hernias resections creation of ostomies and surgical bowel decompression

Paralytic ileus awareness:

Pause a functional obstruction like a paralytic ileus may occur as a complication of intra hospital treatments such as a surgery, opioids, or intra operative fluid resuscitation. an alias can be caused by either intra abdominal or extra abdominal process is many which are prominent in critical care however

 the most common cause of paralytic ileus is due to surgery signs and symptoms of ileus include abdominal distention nausea and vomiting but the pain associated with it is generally less intense and does not have the classic crampy or column the pattern than that of a mechanical obstruction the abdomen is not usually tender unless the underlying causes of inflammatory and upon auscultation it is silent or hypoactive bowel sounds

The progression of postoperative aliases multifactorial bowel function relies on a combination of the enteric and central nervous systems hormones neurotransmitters an inflammatory pathways so the stress of surgery will trigger the stress response -> activation of the sympathetic nervous system which resulted hypoperfusion. additionally the manipulation of the bowels during surgery or localized surgery near or in the abdominal cavity can lead to a paralytic ileus.

 the administration of opioids is great for postoperative pain, however they do slow down intestinal transit by directly affecting the enteric nervous system this in turn affects motility and can exacerbate a paralytic ileus in the postoperative. Intra operative fluid resuscitation can disrupt normal pathways within the gut and alter absorption capacity and affect motility. the use of excess fluids compromises motility because they can contribute to the edema of the bowel wall and in turn decrease motility you may have already heard of the term eras which stands for enhanced recovery after surgery:  promotes develops and publishes skylines for many specific surgeries. it is a multimodal an multidisciplinary approach to care for the surgical patient and a lot of emphasis placed on anticipating assessing an preventing post operative ileus. ERAS has been adopted an integrated into many institutional frameworks in Canada and worldwide and when followed correctly it has been shown to shorten hospital stays by more than 30% and reduce complications up to 50%. the key elements of ERAS protocols include preoperative counseling to provide patient education, pain management, planning, rehabilitation of the patient optimization of nutrition. so some institutions have done away with the rule of NPO at midnight and have instead administered carbohydrate drinks two hours prior to surgery early feeding is encouraged without the need to wait for flatus which is a major change from previous practice management of fluids the goal is to seek a better balance rather than to have the patient be overly positive standardized analgesics an anesthetic regiments which uses opioid sparing and multimodal analgesia an early mobilization they care protocol is based on published evidence such as evidence based modern care changes from overnight fasting to carbohydrate drinks two hours prior to surgery minimally invasive approaches instead of large incisions management of fluids to seek balance rather than large volumes of intravenous fluids avoidance of or early removal of drains and tubes early mobilization and serving of drinks and food the day of the operation

early feeding and advancing diet or adhering to feeding protocols a recent study has shown that no detrimental effects have been associated with early feeding instead it is found to trend towards a lower incidence of anastamosis to Hisense wound infection, pneumonia intraabdominal abscesses and mortality but early oral feeding does increase the risk of vomiting so doesn't this mean we should wait for the bowel to start working before feeding not necessarily it may be helpful to know that the small bowel is typically the least affected after surgery as motility and absorption return to normal within a few hours. stomach emptying is delayed for about 24 hours or more and the colon is the last to recover. early mobilization an early feeding actually improves and stimulates motility, chewing gum increases motility of the gut by stimulating the gastrointestinal hormones as well as the cephalic vagal reflex, this stimulates the first phase of digestion the cephalic phase . more emphasis should be placed on preventing nausea in the 1st place by being attentive to assessments so assessing for distension pain cramping anticipating the appropriate use of prokinetics in antiemetics as ordered ensuring an adequate bowel routine regimen paying close attention to patients who are chronically on opioids encouraging early mobilization making sure patients are sitting up in the chair or upright in bed if unable to ambulate to the chair and keeping track of the fluid balance and looking at hospital policy to limit the amount of fluid you're mixing your medications with you may also notice that places which incorporate eras into their protocol keep fluid boluses at a minimum

MODULE 6: Nutrition

nutrients from foods we eat are chemically converted in our bodies into energy that fuels our internal bodily functions so that all cells and body tissues can be repaired built and well maintained. the six essential nutrients are carbohydrates fats vitamins minerals protein and water. we need minerals to make hormones, build bones, and regulate heart rate. we need protein not only for building and maintaining muscles and connective tissues but also to make enzymes so that these chemical reactions can occur. water is one of our body's most important components as it supports transportation of nutrients and facilitates the chemical reactions that produce energy from food. metabolism is a series of chemical reactions that sustains life and is based on the body's ability to use nutrients an energy . protein carbohydrates and fats that we get from food need to be further broken down by the digestive process because they're not in the right configuration that our bodies can utilize and so these macromolecules are broken down into their subunits. Proteins-> amino acids; carbohydrates->glucose and lipids->fatty acids and in the process energy is released in the form of ATP

These subunits can be used to build up or reconstruct back into macromolecules that are customized to what the body needs however this reconstruction to build up molecules does require energy metabolism consists of these two processes catabolism and anabolism catabolism is the breaking down of macromolecules from food or body tissues into their subunits for the purpose of releasing energy anabolism is the building up and repair process that requires energy.  metabolism is regulated with the help of hormones.

maintain homeostasis this imbalance or deficiency of energy protein and other nutrients could lead to a state of malnutrition which is an inadequate intake of energy protein and nutrients resulting in a change in body composition and diminished function.  it is important to note that malnutrition seen in the hospitalised patient is often a complex interplay between underlying disease. disease related metabolic alterations and reduced nutrient availability either due to poor appetite or impaired absorption.  malnutrition defined in clinical terms includes the following involuntary loss of 10% of usual body weight within six months or involuntary loss of greater than 5% of usual body weight in one month. involuntary loss or gain of 10 lbs within six months body mass index less than 18.5 kilograms per meter squared or greater than 25 kilograms per meter squared chronic disease increased metabolic requirements altered diets or diet schedules and inadequate nutrition intake including not receiving food or nutrition products for greater than 7 days

Malnutrition in hospitalized patients

Guidelines of adequate nutritional support for acutely ill and critically ill patients insufficient delivery of nutritional support and persistent malnutrition continued to exist in the hospital environment. for example the majority of patients and their cute and critical care setting will only receive 60% of their prescribed caloric and protein intake the resultant sub optimal nutrition and negative energy balance increases risk of complications on average malnourished patients have an 8 times higher risk of dying and well nourished patients. they are also more likely to stay in hospital three times longer are four times more likely to develop pressure ulcers under five times more likely to develop catheter associated UTI's if energy protein and nutrients are not available to cells during periods of increased metabolism like in periods of physiological stress the body has to resort to other pathways to increase his glucose production initially the basal metabolic rate is decreased by 20 to 30% and fat becomes the main source for energy where it is broken down into glycerol and fatty acids the liver converts glycogen into glucose and thymine a kind of vitamin B that helps with this conversion. thymine is an essential vitamin which means it cannot be produced by the body and is therefore only available in a dietary form as a last resort amino acids are taken from skeletal muscles for gluconeogenesis this is a key process that results in a major loss of body mass in acutely and critically ill are associated with a catabolic stress state and if not already malnourished before the risk of becoming malnourished in the critical care setting exponentially increases.

the majority of what we consume and what makes up our bodies is water so that's maybe the most vital nutrient then there are vitamins compounds that come in either fat soluble or water soluble forms they aren't used as building blocks are for energy but they're essential in helping the body make use of other nutrients that do those things item in C for example helps improve iron absorption while vitamin K is crucial to blood clotting and some B vitamins are important in the production of ATP from glucose. minerals like vitamins don't provide fuel but they have all sorts of other functions housing magnesium and phosphorus harden bones and teeth while iron is of course crucial in hemoglobin plus potassium sodium and chlorine help maintain your bodies pH balance and are used in action potentials so water vitamins and minerals are all necessary but the three major nutrients: carbohydrates lipids and proteins most of the carbohydrates. ATP being the molecule that your cells used to drive anabolic reactions when they need to make new polymers or get anything else done whether that's operating a sodium potassium pump are detaching the head of a myosin filament to contract a muscle but ATP is too unstable to store so cells often store energy in the form of glucose which they can then catabolized and convert to ATP when they need it now some of your cells can get their energy from fats and many of the most important ones like your neurons in red blood cells feed exclusively on glucose so most of the carbon that your intestines absorb are converted to glucose for that reason but if it's not needed right away that energy can also get stored as glycogen in your liver and muscles or converted to glycerol and fatty acids to make triglyceride fats and even others from kind of marketing war going on against dietary fats we most definitely need them the fats in your adipose tissue store energy of course but they also store fat soluble vitamins and Cushing your organs if it's also form the myelin that insulates the neurons in your brain and throughout your body as well as the oil in your skin and they provide the vital calorie content found in breast milk are there other important lipids like cholesterol which is the precursor to things like testosterone and estrogen and of course phospholipids which form the cell membrane and every single one of the three dozen or so trillion cells you have now if you're into eating meat a lot of the fat you ingest might come from that but guess what plants have fat 2 Lance use lipids for energy storage just like we do except they do it in fruits and nuts and seeds which when you think of it are kind of like plant breast milk it's food for their growing babies either way though when you eat lipids your body breaks down triglycerides into glycerol and fatty acids those molecules can then be processed and used in the making of ATP or they might be converted into other kinds of fatty acids which your cells can then reassemble into your very own triglycerides or phospholipids and your liver happens to be great at converting one fatty acid into another but there are some it just can't synthesize for example Omega six and three fatty acids are called essential fatty acids because your body can't make them so they have to be ingested that turned into all kinds of useful molecules like the ones used for synapse formation in the brain and for signaling inflammation during the healing process but if carbohydrates provide energy and fats insulate and store energy than just about everything else is done with proteins say form the bulk of your muscle and connective tissue but they're also what the ion channels and pumps are made of in your neurons and muscle cells and they make up your enzymes which are responsible for pretty much every chemical reaction in your body in other words your body runs on protein and pretty much is protein nutritionally speaking meets very product eggs lagoons nuts cereals are all particularly high in protein but because everything we eat was once alive and every cell of every living thing contains protein as long as you're eating Whole Foods you're at least partially restocking your protein supplies that might seem like you'd have to eat muscle to make muscle or enzymes to make enzymes but that's not how it works since all your proteins are made-up of just 20 amino acids the differences between the thousands of unique proteins are simply in the sequence of those amino acids and of course you have a specialized molecule that knows just which amino acids to put together in what order to make a certain protein is called DNA when you consume some hamburger for example the protein acting in the meat gets catabolized into its component amino acids which gets mixed up with all of the amino acids from all the other proteins in the meat length of collagen and elastin and tightened in my as in as well as all the proteins from the bond in the tomato in the manage those amino acids then get reassembled using anabolic reactions into your very own but somewhat different proteins as defined by your DNA cell is like a picky little Gordon Ramsey and it has to have every amino acid needed every ingredient present before it will even think about starting to make a protein and just like with your lipids your cells can improvise and convert some amino acids into others if they're missing an ingredient however there are 9 essential amino acids that you cannot make from others and have to eat now lots of foods don't provide every essential amino acid but when you combine foods like beans and rice or pasta and cheese you do get all of the essential amino acids which is important because remember after water you are mostly made of protein on the order of 16%

Effects of malnutrition

Between poor nutrition and poor outcomes in hospitalized patients when you understand the significant role nutrients play in the maintenance of cellular function and this is clearly reflected in the research the greater the caloric deficit the greater risk for developing worse outcomes now think about the acutely or critically ill patient who is already experiencing an imbalance of decreased energy reserves and increasing metabolic demands as the body responds to physiological stress. protein especially forms the bulk of muscle and connective tissue and is involved in almost all cellular functions including the structure of the ion pumps and the nerve and muscle cells to enzymes protein is also extremely important for wound healing immune function and maintenance of muscle mass.

these patients are particularly vulnerable to depleting their protein reserves and can develop a condition called protein energy malnutrition. patients identified with protein energy malnutrition are predominantly prone to the following respiratory failure you can imagine what this means for a patient who is ventilated if muscle wasting continues their ability to be weaned off the ventilator declines, lack of wound healing. For these reasons that institutions have taken steps to better screen promote and assess for safe early feeding to all patients with the help of the interprofessional team supplementing protein has become an integral part of dietary intake in some healthcare settings protein delivery has been combined with exercise and rehabilitation strategies as an opportunity to optimize healing wounds ,supporting immune function, and maintaining lean body mass patients in hospital who are immobile have undergone burn injury or trauma or on paralytic agents can rapidly increase the loss of lean muscle if we can support protein intake and minimize muscle wasting patients will have a better post recovery phase

Nutritional support

nutrition is included as an integral part of recovery feeding not only supports the patient through the stress response but is sought to diminish the metabolic response to stress, prevent cellular injury, and reduce the effects of the immune response.

screening an ensuring that metabolic demands are met is essential and often requires an interprofessional team approach risk for malnutrition should be assessed upon admission as some patients may arrive already malnourished on going assessment is required to ensure energy requirements are being met this involves advocating for early feeding which means that nutritional status has been discussed and a plan is in place this becomes particularly important for patients in the step down unit or ICU where feeding should be initiated within 24 to 48 hours of admission unless otherwise contraindicated ideally the patient has already been hemodynamically stabilized and fluid resuscitated if necessary goal rate should be reached within 48 to 72 hours

 there are two options of feeding methods enteral nutrition or nutrients are provided by way of the gastrointestinal system and parental nutrition or nutrients are provided intravascularly. enteral nutrition is the delivery of feeds directly into the GI tract via tube that is placed into the stomach duodenum or jejunum. enteral feeding is the preferred route for all patients who have a functional an accessible GI tract because it is more physiologic than parental nutrition it can be used to supplement or substitute nutrition for those who have a low appetite or those who cannot take oral feed safely. there is a large variety of formulations provided by different companies to suit the needs of the patient naso enteral tubes are the most popular in the acute and critical care setting however if the upper GI tract is inaccessible due to mechanical or absorptive dysfunction post π lorick feeding that is duodenal or jejunal enteral feeding can be done too but if recovery is expected to last months a more permanent feeding tube is inserted percutaneously through the abdomen into the stomach or jejunum guided by radiography or fluoroscopy continuous feeds are preferred over bolus feeds to avoid risk of aspiration and reduce fluctuations in glycemic control the expected duration of nutritional support the patients condition and most importantly the GI tract function an ability to absorb nutrients is considered when deciding placement technique and the kind of two being utilized.

the absence of enteral feeding in the malnourished hospitalised patient can lead to the following: mucosal atrophy leading to the loss of integrity of the gut mucosal barrier which increases permeability and decreases absorptive capacity of the gut a reduction of mucosal blood flow and therefore atrophy of lymphoid and cell structure which reduces gut immunity if no mucus is being produced the bacteria can easily adhere to the epithelial lining which potentially perpetuates sepsis for those patients receiving enteral feeding as their source of nutrition in acute and critical care settings the average patient received only 60% of their prescribed caloric intake and provisional protein is the largest deficit So what happened to that missing 40% think of all the delays that occur in your unit or that you've seen or experienced first there can be the delay of tube insertion depending on the tube there may be specific personnel required to insert it nasogastric orogastric and post π lorick tubes also require confirmation of placement and if the best option is a per cutaneous feeding tube the patient will need to wait for space an available personnel to likely place the tube in interventional radiology then there's the delayed initiation of the order to begin feeding and the time it takes to reach daily goal rates or daily volume intake depending on the patient's tolerance and acuity level this may take a few days however research shows that the two main barriers responsible for acquiring adequate intake of nutrients to meet metabolic demands is the perceived fear of the risk associated with aspiration and disruptions and continuous feeding during patient care routines anticipated diagnostic tests and procedures or transportation off the unit having just covered the barriers related to meeting total caloric and protein intake in the acute and critically ill let's now focus on the nursing considerations and interventions click on each barrier to learn what you can do to improve delivery of nutrition to acute an critically I'll patients

Parenteral Feeding:

Chemical formulation that is given directly into the bloodstream by an intravenous catheter this nutrition includes protein carbohydrates fats minerals electrolytes and vitamins studies have shown that parental nutrition does not stimulate the same physiologic response as enteral nutrition and is therefore only required in patients who have non functional or malabsorptive GI tracks for example patients with bowel obstructions short bowel syndrome or GI officials the preferred route for parental nutrition is via central vascular access device receive add but it can also be given peripherally if peripheral access is the only route available a large for Ivy catheter is required if using a sieve add a dedicated catheter lumen must be used because of the high risk of infection associated with parental nutrition even if a previously used line is being accessed careful monitoring must be done for the development of line infection so checking the site using aseptic technique and regular flushing to maintain patency is very important when caring for the line parental nutrition is tailored to the patients needs and his initiation is ordered by the physician a dietitian provides the calorie requirements based on their assessment and calculations and then pharmacy prepares the individual formulations the addition and revision of electrolytes in each parenteral nutrition bag is evaluated every day based on daily blood work and fluid status each institution will have their own policy regarding the timing of drying blood for patients receiving parental nutrition complications associated with parental nutrition are outlined in the table that can be viewed when you click on the green button

Refeeding Syndrome:

can occur with any form of nutritional intake whether it be oral enteral or parental refeeding syndrome occurs when malnourished patients experience fatal shifts in fluids and electrolytes after receiving oral enteral or parental nutrition. these shifts can cause serious clinical harm to the patient including diarrhea heart failure coma and even death.  in states of malnutrition the body is starved of glucose and switches from using carbohydrates and will look to other sources of energy the body starts to use fat and protein as a main energy source in an effort to generate ATP.  intercellular minerals are also often depleted during starvation so when a malnourished individual suddenly begins to be refed and receives nutrition there is a sudden increase in glucose resulting in an increase in insulin and decrease secretion of Glucagon increased insulin will result in bring glucose into the cells but will also shift electrolytes into cells as well because minerals are required in the synthesis of glycogen fat and proteins this process specifically causes the decrease of phosphate magnesium and potassium which are already depleted from the period of starvation therefore hallmark signs of refeeding syndrome are hypophosphatemia which is the most common characteristic hypomagnesemia and hypokalemia signs and symptoms of refeeding syndrome are mainly related to the depletion of electrolytes leading to arrhythmias seizures hypotension cardiac failure and diarrhea water retention also occurs likely as a result of decreased renal excretion of sodium in water which can lead to peripheral edema congestive heart failure or other cardiac arrhythmias

Considerations for refeeding

For those patients at high risk for refeeding syndrome it's very important to closely monitor electrolyte levels when feeding is initiated any patient who has had minimal food intake for five or more days is considered to be at risk for refeeding syndrome patients considered at risk should undergo a thorough nutritional assessment before starting enteral feeds or parental nutrition electrolytes phosphate potassium magnesium and sodium as well as glucose should be measured at baseline and regularly throughout feeding and treat as necessary nutritional support should be restarted slowly an adjusted to each patient's clinical needs cardiac monitoring should be applied due to the increased risk of cardiac arrhythmias due to repeating if refeeding syndrome is detected the rate of feeding will likely be slowed down and electrolytes will be replaced As for the physician and the specialist dietetics team