Heat/Cold/Endocrine
1. Heat and Cold Emergencies
Hypothermia
- Mild Hypothermia – Core body temperature is between 32°C and 35°C
o The mnemonic used: Fumbles, stumbles, tumbles, and grumbles.
o Conscious and shivering
- Moderate hypothermia – Core body temperature 28°C – 32°C
o Impaired consciousness may or may not be shivering. ‘
o Active external rewarm
o Minimal movements to avoid arrhythmias
- Severe Hypothermia – core body temperature is less than 28°C.
o Altered LOC, unresponsive and or cardiac arrest.
o Treat in ECMO/CPB center (may reduce Pt mortality by 40-90%)
- Hypothermic Cardiac Arrest
o Possible below 32°C, increased risk below 28°C and continues with ongoing cooling
o Treatment: CPR and up to 3 doses of EPI (0.1mg/mL) and defibrillation
Cold Physiology
- Below ~ 29°C pupils become dilated and fixed
- Below ~ 23°C, corneal reflexes may be absent.
- Note: Pupil responses are not reliable for neurologic prognosis in hypothermia
Osborn J waves
- Usually occurs in mild hypothermia, below 32°C
-
Metabolic changes
- Cold Diuresis: the renal response to hypothermia
o Vasoconstriction-induced hypervolemia (vasoconstriction pushes fluid into the cellular space, causing hypervolemia).
Heat Emergencies
The body has several ways to dissipate heat to the environment, including radiation, conduction, convection, and evaporation.
The physiological response to heat stress occurs through four primary mechanisms: dilation of blood vessels, primarily in the skin; increases in sweat production; decreased heat production; and behavioural heat control.
Prickly heat – a pruritic, maculopapular, erythematous rash. The sweat pores become blocked, causing sweat ducts to become inflamed.
Heat Cramps are painful, involuntary spasmodic contractions of skeletal muscle that happen when a person sweats profusely, loses electrolytes and replaces fluid losses with water or another hypotonic solution (sugar water) instead of electrolytes. Ringers is better than normal saline. Do not give D50; the sugar will make it worse.
Heat stress
- Exhaustion – results from 2 different ways either:
o Water depletion – occurs in the elderly or in people in hot environments with inadequate water replacement.
o Salt depletion – occurs in unacclimatized individuals who replace fluid losses with large amounts of hypotonic solution (i.e., sugar juice, pop)
- Body temperature usually does not go above 40°C
Heat Stroke
- Hyperthermia (> 40°C) and altered mental status
- CNS is vulnerable – Cerebellum highly sensitive to heat; ataxia is an early neurologic finding
- Treat by spraying Pt with water and providing airflow, place wet towels or sheets over Pt's body or place ice on, if hypotensive Bolus of NS (1-2 L)
- Early complications:
o Hypotension (low cardiac output and elevated central venous pressure need vasoactive catecholamines (if 20cc/kg bolus of NS does not work, then Dopamine (B1 effects) (5-10mcg/Kg/min) or Dobutamine is required)). The use of Norepi may impede cooling by redirecting blood flow away from the skin (A1 effects).
o Fluid and electrolytes
§ Vary due to onset and duration, previous medication history (such as diuretics) and underlying comorbidities (such as cardiovascular)
§ Hypokalemia is possible due to total body depletion of potassium
§ Hyperkalemia seen in acute renal failure and rhabdomyolysis
§ Hypernatremia seen in severely dehydrated patients
§ Hyponatremia due to PO hydration of hypotonic solution
o Thermal injury
§ Can cause increased platelet aggregation, changes in capillary permeability, and deactivation of plasma proteins (further causing a decrease in clotting factor, DIC, and fibrinolysis)
§ Can occur 24-72 hrs. post-injury.
o Thermal injury to the Liver:
§ Common finding in heat stroke
§ Jaundice doesn’t always develop
§ 24-72 hrs post thermal injury is when hepatic enzyme levels elevate due to centrilobular necrosis
§ Glucose levels are affected here (check the patient's BGL)
§ Hepatic damage is almost always reversible with full recovery
o Renal Failure
§ Is due to thermal injury to the kidney, rhabdomyolysis or volume depletion
§ S/S oliguria (low urine output)
§ Early fluid replacement is required as it decreases the detrimental effects of heat stroke.
o ARDS – requires ventilatory support
o Myocardial injury may also occur in heat stroke (ECG monitoring and lab values are key)
o Seizures may be present when cooling the patient (treat with benzodiazepines)
o The presence of hypotension, low cardiac output and falling cardiac index is associated with poor prognosis and patient outcome.
2. Submersion, Vesicants, High Altitude Syndromes
Vesicants
- An agent that induces blistering (used in chemical weapons, sulphur muster)
- Cause damage to eyes, skin, mucous membranes and lungs if a Pt is exposed to high concentrations
- Treatment – flushing the affected area with copious amounts of water (20 minutes under a shower)
Drowning – Submersion in a liquid medium resulting in respiratory difficulty or arrest. Drowning is the process of experiencing respiratory impairment from submersion in liquid.
Pathophysiology of Drowning
- Following submersion in a liquid medium, the Pt first voluntarily holds their breathing. The Pt must breathe and then starts to swallow small amounts of water and may start to aspirate; a laryngospasm occurs, which constricts the airway. This can cause a dry drowning (rear). The laryngospasm will break, and the Pt will start to inhale the water, carbon dioxide levels will increase, oxygen levels will decrease, loss of consciousness, multi-system organ failure, and then death will occur.
Treatment
- Conscious – Oxygenate, consider CPAP @ 5cm H20
- Unconscious – BVM with 100% oxygen consider PEEP @ 5cm titrating to a max of 10cm H2O. Consider ET intubation and positive pressure ventilation if necessary.
Boyles Law
- The volume of a gas is inversely proportional to its pressure
Dalton’s Law
- The total pressure of a gaseous mixture is equal to the sum of the partial pressure of each of the individual gas mixtures.
Henry’s Law
- Solubility of a gas in a liquid at a particular temperature is proportional to the pressure of that gas above the liquid.
Charles’s Law
- All gases will expand equally when heated.
Barotrauma
- When air pressure in hollow spaces of the body rises too high or drops too low. (the squeeze)
Decompression Sickness (DCS)
- Refers to a broad range of signs and symptoms caused by nitrogen bubbles in the blood and tissues coming out of solution during accent
- Nitrogen gas bubbles are produced and accumulated in blood and tissues as a result of rapid ascent during dive.
- Acts as air embolism in the bloodstream.
- Severe pain, usually in joints and abdomen
- Type 1 decompression sickness
o Mild form that affects skin, lymphatic and musculoskeletal systems
o Joint pain is the most common symptom
o Skin may be become mottled and pruritic
- Type II decompression sickness
o Caused by nitrogen bubbles in all other systems, but especially the nervous, respiratory, and circulatory systems.
Arterial Gas Embolism
- If ascent occurs to rapidly or if a diver holds their breath, nitrogen bubbles will form in the arterial bloodstream.
Nitrogen Narcosis
- State of stupor resulting from nitrogen’s effect on cerebral function (may act intoxicated)
PaO2 – the pressure of dissolved in your blood
SaO2 – in oxygen saturation as measured by blood analysis
SpO2 – % of hemoglobin bound to hemoglobin
High Altitude Syndromes
Altitude illness is a problem of hypoxia due to a decrease in or low atmospheric pressure. Three illnesses associated with an ascent to altitudes 8,000 ft or more above sea level
Acute Hypoxia
- Occurs in the event of sudden and severe hypoxia insult. (sudden decompression of an airplane)
Acute Mountain Sickness
- A person ascends to an altitude of 2,000 meters (6,600) too rapidly. Will present with a headache and a combination of
o Nausea or vomiting, dizziness, fatigue, sleep disturbances
- Treatment – prevent progression, treat symptoms and descend.
High Altitude Pulmonary Edema (HAPE)
- Noncardiogenic, accumulating fluid in the lungs due to high altitude. The heart function of the left ventricle is not affected. Occurs at altitudes of 2,500 meters or greater
High Altitude Cerebral Edema (HACE)
- Increase of fluid in the brain leads to increased intracranial pressure. Progressive neurologic deterioration or ataxia in an individual who has recently ascended to a high altitude.
- S/S altered LOC, ataxia, stupor, coma, increased ICP can result in paralysis of CN # 3 (oculomotor), 6 (facial)
Lightning Injuries
Voltage
- Measurement of energy within an electric circuit at a given point.
Current
- Flow of electric charge through conductive material
- Current referenced by a unit of measure called amperes
- Voltage and current of lighting is extraordinarily high – in excess of 1,000,000 volts with 200,000 amperes of current
- Direct strike
o Lighting hits the victim first before making contact with any other objects
- Contact strike
o Lighting hits the object with which the Pt is in contact
- Side flash strike
o Lighting hits an object and then jumps to the victim, who is located nearby
- Ground current strike
o Lighting energizes the ground, affecting people standing in an area of the strike
- Be alert for associated traumatic injuries
3. CO Poisoning
- Naturally occurring in the body due to the breakdown of heme. Normal levels in the human body are approx. 1% in non-smokers and 4-10% in smokers
- Binding affinity to hemoglobin is 200 times that of oxygen
- Binding is higher in Fetal hemoglobin, which may account for more severe fetal toxicity levels in babies.
- Unusual source of CO poisoning is Methylene Chloride found in: varnishes, paint strippers, bubbling fluid in Christmas ornaments
- Half-life of Carboxyhemoglobin (COHb):
o On room air at normal atmospheric pressure: 249-320 minutes
o 100% oxygen at atmospheric pressure: 74-80 minutes
o If carboxyhemoglobin is generated by methylene chloride is up to 13 hours due to the ongoing metabolic production in the body
- As Carboxyhemoglobin levels increase it causes:
o Relative anemia
o Hypoxia
o Shift oxygen dissociation curve to the left (impairing O2 release to the tissues)
Carbon monoxide poisoning
- Decreases hemoglobin saturation
- Shifts oxygen dissociation curve to the left
- Cardiac injury and dysfunction result as CO levels rise in the body
o Myocardial infarction, cardiomyopathy, myocardial fibrosis
- Damaged endothelium will attract neutrophils and trigger an inflammatory cascade, causing neurologic injury and dysfunction seen primarily in the CNS
o The brain’s basal ganglia are super sensitive to CO toxicity and lesions may show on MRI or CT scans
- Clinical effects of carbon monoxide:
o Rhabdomyolysis (causes your muscles to break down (disintegrate), which leads to muscle death. When this happens, toxic components of your muscle fibers enter your circulation system and kidneys)
o Acute MI
o Neuronal cell death
o Basal ganglia in the brain are very sensitive to CO and may show Lesions on CT imagining
- Mild/Moderate Poisoning
o Mild fever, tachycardia, tachypnea, hypertension/hypotension may be seen, mild headache, confusion-irritability, focal neuro deficits, ataxia, coma
- Severe Poisoning
o Retinal hemorrhage, respiratory or cardiac arrest
Cyanide Poisoning
- Inhibits many metabolic processes in the body (blocks the 4th complex of the oxygen cytochrome oxidase in the Kreb cycle
- The most severe effects come from interfering with mitochondria and stopping cellular respiration
- ATP production is stopped, and organs and tissues with high oxygen consumption demands are the first and most severely affected (brain, heart, lungs)
5 elements will determine the clinical presentation of the patient:
- What was the cyanide-containing compound?
- What is the route of exposure?
- What is the concentration to which the patient was exposed?
- What was the duration of exposure?
- What is the time since the exposure?
The cherry red skin results from veinous hemoglobin and oxygen saturation increasing because cellular respiration is blocked. The compensatory mechanism is to supersaturate oxygen because we have more oxygen in the veinous system the skin tends to turn red
- Suspect this poisoning anytime patients have been exposed to combustible materials
- Median lethal dose (LD50) for hydrogen cyanide gas is estimated to be 200 ppm for 30 minutes of exposure or 600-700 ppm for 5 minutes of exposure
- The two most common exposure routes are inhalation and ingestion (potassium cyanide, sodium cyanide)
Cyanide poisoning Treatment
- The two antidotes are used for Cyanide Toxicity; the most commonly used is:
o Treatment #1
§ Hydroxocobalamin (Vitamin B12a)
§ It is a metal protein that has a cobalt center; the cyanide binds to the cobalt center and removes it from the cytochrome oxidase, and allows the mitochondria to reactivate the electron transport chain (Kreb cycle). It forms cytocobalmin and its cytocobalmin that can be excreted through the kidneys
o Treatment #2
§ Cyanide antidote kit
· 10 mL vials of 3% sodium nitrate (300mg) IV
o The nitrates create methemoglobin. It binds to the cyanide, removes it from the cytochrome oxidase, and allows the mitochondria to reactivate the electron transport chain (Kreb cycle).
o
· 50 mL vial of 25% sodium thiosulfate (12.5g) IV
o Enhances the activities of the enzyme rhodanese (helps to transfer of sulfate from sodium to cyanide to create thiocyanate) Thiocyanate then gets excreted by the kidneys in a less toxic form.
Cyanide Poisoning Treatment Criteria
- Knows or suspected risk factors and when one or more of the following:
o GCS less than 8
o Systolic BP < 90 mmHg (late sign)
- Or
o GCS <14 with one or more of the following:
o Chest pain/ischemic ECG changes
o Dyspnea and / or pulmonary edema
o Respiratory rate < 12 (late sign)
Knowing or suspected Cyanide Poisoning:
- Seizing / Cardiac Arrest
o 5g Hydroxocobalamin IV/IO
- All other patients
o 5g IV/IO over 15 minutes
- Mandatory OLMC to give a repeat 5g does for a total max 10g
4. General Endocrine Emergency
The endocrine system is responsible for numerous long-term processes or functions within the human body. This system is composed of glands and organs that secrete a variety of hormones or chemical messengers
Hormones affect individual body cells and regulate body functions
Some of the major processes controlled by the endocrine system include:
- Regulation of metabolism and electrolyte composition
- Response to stressors
- Growth and development
- Reproduction
The Endocrine system releases a variety of hormones, including:
- Releasing hormones – hormones which stimulate a body response or act on other endocrine glands, causing them to release hormones
- Inhibiting hormones – inhibiting the release of other hormones via negative feedback
- With few exceptions, the Endocrine System is regulated by Negative feedback
The Endocrine System
- Only cells which have a receptor for specific hormone molecules are affected by the presence of that hormone
- Hormones cause cellular changes by binding to receptors on these target cells
o The number of receptors on a target cell can increase (up-regulation) or decrease (down-regulation) in response to hormonal activity
o Hormones are also able to directly affect cells through intracellular hormone receptors or affect cells indirectly through hormone receptors on plasma membranes
- The endocrine system plays a crucial role in maintaining homeostasis
- Endocrine emergencies are often triggered by an event or stressor, such as an acute infection
- An endocrine emergency may be the initial presentation of an underlying, or as of yet, undiagnosed endocrine disorder for patients
o Most urgent endocrine problems in terms of prehospital care include dysfunction of the following organs:
§ Pancreas
§ Thyroid
§ Adrenal glands
Primary disorder
- Dysfunction can involve the endocrine organ itself, under-stimulation or overstimulation by the pituitary (secondary disorders), or rarely because of abnormal tissue responses to hormones (usually hypofunction)
The Endocrine System – The Pancreas
- The pancreas has both exocrine and endocrine functions
- The primary endocrine function of the pancreas is to maintain healthy blood glucose levels
o This function involves the pancreatic islet cells (or islets of Langerhans)
o The Islet Cells produce and release hormones directly into the bloodstream
- The two pancreatic hormones involved with blood glucose levels are
o Insulin (produced by Beta cells)
o Glucagon (produced by Alpha cells)
- Diabetes Mellitus (DM) is a chronic disease which occurs as a result of pancreatic dysfunction
o The Pancreas does not produce enough insulin or
o The body cannot effectively utilize insulin
o Two types of Diabetes Mellitus account for the majority of cases – Type 1 and Type 2
- Terms to know
o Hypoglycemia
o Hyperglycemia
o Glycogenesis – creation of glycogen stored in the liver
o Gluconeogenesis – a metabolic pathway that results in the biosynthesis of glucose from certain non-carbohydrate carbon substrates
o Glycogenolysis – break down of glycogen to glucose-1-phosphate and glycogen
- Pancreas and blood glucose level (BGL)
o Brain cells
§ Need constant glucose-Glucose is the main energy source of the brain
§ Cannot quickly convert to using fats
§ Hypoglycemia: life-threatening emergency
· Can cause brain damage or death
§ Other cells
· Can use fat as a source of energy but inefficiently
o Glucagon
§ Secreted when BGL is low
§ Accelerates glycogenolysis (creation of glycogen stored in the liver)
§ Stimulates gluconeogenesis (a metabolic pathway that results in the biosynthesis of glucose from certain non-carbohydrate carbon substrates)
§ Enhances glucose release into the blood
o Insulin
§ Secreted when BGL rises
§ allows glucose to enter the cell
The Endocrine System – The Thyroid Gland
- The thyroid is a small gland located in the neck, just inferior to the thyroid cartilage and cricoid cartilage
- Thyroid hormone (T3 and T4) levels are controlled through a complex feedback loop
- The hypothalamus releases thyrotropin-releasing hormone (TRH), which triggers the pituitary gland to release thyroid-stimulating hormone (TSH), which stimulates the thyroid gland to release T3 and T4
- Thyroid hormone is the major metabolic hormone within the body
o With the two main hormones released being
§ Thyroxine or tetraiodothyronine (T4)
§ Triiodothyronine (T3), which collectively makes up the thyroid hormone
- Thyroid hormone has numerous effects on the body, including
o Increased heart rate (chronotropy)
o Increased strength of contraction of the heart (inotropy)
o Increased rate of peristalsis (food passing through the gastrointestinal tract)
o Gluconeogenesis
o Glycogenolysis
The Endocrine System – The Adrenals
- Adrenal cortex – secretes a variety of hormones
o Mineralocorticoids – controls electrolyte balance
o Glucocorticoids – affect glucose metabolism
o Androgens are male hormones/precursors to estrogens
- The adrenal medulla
o Secretes the hormones epinephrine and norepinephrine
§ Secreted in response to sympathetic nervous system stimulation
§ Fight or flight response
- Endocrine emergencies include
o Hypoglycemia
o Diabetes
o Diabetic ketoacidosis
o Hyperosmolar hyperglycemic nonketotic syndrome
o Hyperthyroidism and thyroid storm
o Hypothyroidism and myxedema coma
o Adrenal insufficiency and adrenal crisis
Endocrine Disorders
- Causes
o Hypersecretion or hyposecretion
o Hypersecretion leading to excessive target-gland activity
o Hyposecretion resulting in under activity of the organ
- Effects are determined by
o Degree of dysfunction of the gland
o Age, sex and underlying health of the patient
o Dysfunction ranges from barely detectable to extreme dysfunction
Endocrine Emergencies
- Scene assessment
- Initial assessment
- Focused history
- Detailed physical exam
- Ongoing assessment
Endocrine Emergencies – Scene Size-up
- Standard operation and ongoing assessment
- Clues may be evident – medication, insulin pens, syringes, or pumps, poorly healing wounds, limb amputations
- General Appearance
- Chief complaint
- Common presentations include:
o Altered metal status
o Weakness
o Fatigue
o Palpations
o Fever
o Abdominal pain
Primary Assessment
- Level of responsiveness (LOC or AVPU)
- ABCs
- Need for oxygen
- Unresponsive or compromised airway, breathing or circulation is critical – Treat any life threats immediately
- Once life threats have been dealt with, further appropriate treatment can be determined
- A – Alcohol, acidosis (metabolic disorders), ammonia (hepatic encephalopathy), arrhythmias (any cardiac causes)
- E – Endocrine, electrolytes, encephalopathy
- I – Infection
- O – Oxygen, overdose/opiates
- U – uremia
- T – trauma, temperature (hyper/hypothermia), thiamine (Wernicke-korsakoff)
- I – Insulin (hypo/hyperglycemia)
- P – Poisoning (all medication), psychiatric
- S – stroke, seizure (postictal state), syncope, space-occupying lesions, shunt (VP) malfunction
Treatment
- Will be determined by assessment findings and history
o For most endocrine emergencies, prehospital treatment will involve a standard approach and ongoing assessment
o maintenance of Airway, Breathing, and Circulation
§ serial set of vitals signs – RR, HR, BP. BGL, O2, temp
§ cardiac monitoring – 12 lead ECG
§ IV initiation and fluid to maintain perfusion
§ Specific treatments for hypoglycemia within the PCP scope will include the use of
· Oral glucose, D50W and Glucagon
Ongoing assessment
- Obtain medical history, a minimum of SAMPLE- from patient or bystanders
- Tailor your questions for follow-up on the chief complaint
- Obtain vital signs, pulse oximetry, and blood glucose level
- Perform rapid physical exams on critical patients
- Perform focused exam on noncritical patients
- Continue to reassess the patient frequently
Thyroid Emergencies
- Hyperthyroidism occurs when the thyroid gland secretes excess thyroxine (increases the body's metabolic rate)
- Most commonly caused by an autoimmune disorder – Grave’s disease
- Other causes include
o Thyroid or pituitary tumors
o Inflammation of the thyroid and
o Excess intake of iodine
- Less frequent causes include
o AMI
o Major infections
o Thyroid trauma
o Salicylate overdose
o Diabetic ketoacidosis
o Congestive heart failure
o Pulmonary embolism
- Thyroid storm
o Occurs as a result of very high levels of circulating Thyroxine (T4)
o Signs include
§ Altered mental status
§ Hypotension
§ Tachycardia
§ Tachypnea
§ Hyperthermia with hot diaphoretic skin
§ Blood sugar levels may be low, and the patient may be dehydrated due to nausea, vomiting and diarrhea associated with the thyroid storm
Hyperthyroidism and Thyroid Storm
- Prehospital treatment for thyroid storm is supportive
- Standard approach and ongoing assessment
- Maintaining airway, breathing and circulation – oxygenation and ventilation PRN
- IV access and fluids and dextrose PRN
- Cardiac monitoring – 4-lead and 12-lead ECG
- Cooling measures if hyperthermic
- Ongoing assessment and history gathering
- Treat underlying cause if possible (for tachycardia, propranolol is the drug of choice because it blocks the T4 transformation to T3. If tachycardia and hypertension, we only have metoprolol to slow the heart rate)
- Rapid transport
Hypothyroidism and Myxedema Coma
- The thyroid gland fails to secrete an adequate amount of thyroxine to support the body’s metabolic requirements
- S/S are the result of decreased metabolism and include
o Chronic fatigue
o Cold intolerance
o Headache
o Weight gain
o Constipation
- Myxedema Coma involves severe hypothyroidism
o Life-threatening
o Presentation may include
§ Altered mental status – patients may range from confused to unconscious
§ Slow respiratory rate
§ Bradycardia
§ Hypotension
§ Hypothermia
- Prehospital treatment for a myxedema coma is largely supportive – standard approach and ongoing assessment
o Maintaining airway, breathing and circulation as required
o Cardiac monitoring, 4-lead and 12-lead ECG
o IV initiation and support perfusion PRN
o Ongoing assessment and history gathering (SAMPLE)
o Rapid transport
Adrenal Insufficiency and Adrenal Crisis
Adrenal insufficiency is most commonly seen with Addison’s Disease.
- Addison’s disease is often a result of autoimmune disease
- Decreased aldosterone and cortisol (not pushing salt into the blood, causing hyponatremia and hyperkalemia
- Signs and symptoms of adrenal insufficiency may develop gradually and can be non-specific, including
o Nausea and vomiting
o Diarrhea
o Fatigue
o Abdominal pain
o Muscle weakness and joint pain
o Hypotension
o Hypoglycemia
- History will be key
- Adrenal crisis is a sudden severe worsening of symptoms associated with adrenal insufficiency, including but not limited to:
o Abdominal pain
o Dehydration
o Nausea and vomiting
o Diarrhea
o Hypotension
o Hyperpigmentation of skin (exposed and nonexposed)
o Altered mental status
o And adrenal crisis may be triggered by illness, injury or exposure to stressful situations
o Key points
§ Signs and symptoms of Addison’s disease often develop gradually, and are often develop gradually, and are often vague or non-specific
§ Suppression of the adrenal glands can occur regardless of the route steroids are given – topical, oral, intrathecal, or inhaled
o Presentation can include
§ Syncope,
§ Seizures
§ Hypoglycemia and cardiac dysrhythmias
§ Hyperkalemia and acute hyponatremia can cause seizures and cardiac dysrhythmias
- The most common cause of adrenal insufficiency and adrenal crisis is due to adrenal suppression from prolonged steroid use when
o The patient abruptly stops taking their corticosteroid medication
o As a result of increased physiologic stress because of illness, injury or surgery
- Prehospital treatment for adrenal or Addisonian Crisis is largely supportive – standard approach and ongoing assessment:
o Maintaining airway, breathing and circulation as required
o Cardiac monitoring, 4-lead and 12-lead ECG
o IV initiation and support perfusion PRN
o Ongoing assessment and history gathering (SAMPLE)
o Serial vital signs and managing BGL
§ Consider adrenal crisis in patients who does not improve with dextrose
o Rapid transport – patient requires steroids
Adrenal Excess – Hypercortisolemia or Cushing’s Disease
- Cushing’s syndrome refers to excess cortisol of any etiology
- Cushing’s syndrome can be endogenous (the body produces too much cortisol)
- Exogenous, which is the most common and results from the long-term use of glucocorticoid or steroid medications (these medications are also used to treat asthma, rheumatoid arthritis and Lupus)
- Cushing’s syndrome has multiple effects on bone metabolism (pathologic fractures may occur as a result)
- Other signs and symptoms include
o Weight gain
o Thin arms and legs
o A round face
o Increased fat around the base of the neck
o A fatty hump between the shoulders
o Easy bruising
o Stretch marks on the abdomen, breasts, hips and under the arms
o Weak muscles
- Prehospital treatment for is largely supportive – standard approach and ongoing assessment:
o Maintaining airway, breathing and circulation as required
o Cardiac monitoring, 4-lead and 12-lead ECG
o IV initiation and support perfusion PRN
o Ongoing assessment and history gathering (SAMPLE)
o Serial vital signs
o Consider possible fractures – splint appropriately
o Transport
5. Endocrine Emergencies
Type 1 Diabetes Mellitus
- “Autoimmune, cellular-mediation destruction of Beta cells of the pancreas.”
- There are three main cells within the Islets of Langerhans of the pancreas:
o Alpha cells: secrete the hormone Glucagon (causes catabolism-breakdown of glycogen, proteins and fats to form glucose).
o Beta cells: produce insulin – causes anabolism (stores glucose as glycogen, proteins and fats).
o Glucose enters the beta cell and, with the mitochondria, makes an increased amount of ATP. This causes the closure of the potassium channels; potassium cannot leave the cell, and it causes calcium to be released, which causes the vesicles holding the insulin to migrate to the cellular membrane and release the insulin
o Delta cells: secrete the hormone Somatostatin
o Antagonizes the alpha and beta cells, suppressing pancreatic hormones, including insulin and glucagon
General Facts
- Accounts for only 5% of diabetes cases
- Most diagnosed in children and young adults
o Immunemediated destruction of Beta cells
o Spontaneous ketoacidosis almost always develops in untreated cases, and insulin is required for survival
§ There are 3 things we need to look at
· Osmolality
· Dehydration
· Acidosis
o Usually develops in a day and does not take a high level of sugar to develop
Pathology
- High point of lymphocytic infiltration and destruction of beta cells in the pancreas
- As beta-cell mass declines, insulin secretion decreases until the available insulin is no longer adequate to maintain normal blood glucose levels
o If we don’t have the insulin to help transport the glucose into the cell, we can use other mechanisms to create the energy through glycolysis.
- Resulting in hyperglycemia
- Usually the people affected are not obese and usually present initially with diabetic ketoacidosis (DKA)
- Onset of symptomatic disease is sudden and is not predisposed by eating a meal
Classic signs and symptoms include:
o Polyuria
o Polydipsia (extreme thirst)
o Polyphagia (abnormally strong, incessant sensation of hunger or desire to eat, often leading to overeating)
o Unexplained weight loss
o Other symptoms may include fatigue, nausea and blurred vision, poor healing, diabetic foot
Treatment
- #1 treatment is insulin
o Insulin can be administered in various forms (intermitted dosing, IV infusion, continuous subcutaneous infusion (insulin pump))
- Patients may also require
o Beta Cell transplantation
o Pancreas transplantation
o Combined kidney/pancreas transplantation
Type 2 Diabetes Mellitus (T2DM)
- Complex heterogeneous metabolic disorder characterized by chronic elevation of plasma glucose levels
- As sugar levels rise, the sugar continues to rise, continuing to hammer the betta cells, and the beta cell reacts to the high levels of sugar and produces even more insulin and that chronic extra production of insulin stresses the betta cell out.
- There is some insulin production, but the problem is the insulin resistance or decreased insulin production
- Over an extended amount of time, the osmolarity would start to change in the blood; we will see ion shifts and glucose. Because of that, that osmolarity we are starting to draw more fluid from the tissues
- We will see a nonketotic hyperosmolarity hyperglycemic state, and the blood sugars will be incredibly high, in excess of 44 mmol.
- When we look at diabetic ketoacidosis, quite often, they are not even that high; they might only be in the 30 mmol
- When type 2 becomes acidotic, it is a progressive disorder that happens over days, and all of these fluid and osmolality shifts start to affect the central nervous system and cause cerebral edema and eventually cause seizure, coma, and death.
General Facts
- Major public health issue worldwide
- Chronic metabolic disorder
- Reduces like expectancy by 10 years in patients
- Increased risk at younger age due to obesity and lack of physical exercise
- Characterized by hyperglycemia with relative deficiency of insulin production and a reduced response of target tissues to insulin
Signs and Symptoms are generally mild and nonspecific and include:
- Fatigue
- Weakness
- Polydipsia (extreme thirst)
- Polyphagia (abnormally strong, incessant sensation of hunger or desire to eat, often leading to overeating)
- Blurred vision
- Most people are overweight, over 30 years of age, and have other comorbidities (HTN, cardiovascular disease, dyslipidemia, polycystic ovary syndrome
- PMHx: superficial infection and slow healing skin lesions after minor trauma are a RED FLAG for T2DM
Treatment
- Consists of 3 different categories:
o Day to day prevention of hyperglycemia
o Prevention and management of chronic complications
o Acute therapy of severe hyperglycemia and life-threatening metabolic decompensation (HHNK, DKA)
o Insulin-dependent diabetics have to manage choleric intake to take enough insulin and monitor the amount of activity.
Antidiabetic Pharmacotherapy
- The classification of the drug is based on the mechanism of action
- Agents that cause insulin sensitization primarily in the liver (metformin)
o Makes the liver more sensitive to insulin thinking that the insulin levels are hight and thinks sugars are high and to stop releasing sugars
- Agents that promote secretion of insulin (the “ides” from the beta cells)
- Agents that block the reabsorption of glucose by the kidney
- Agents that slow absorption of carbohydrates (can decrease/increase the amount of glucose that is urinated ??
Antihyperglycemic Agents
- 9 classes exist:
o Sulfonylureas: Potentiate insulin secretion (can produce hypoglycemic states)
§ Medication example: glyburide, glipizide
o Biguanides: suppress liver glucose production (can not cause low BGL increases the liver sensitivity)
§ Medication example (metformin)
o Glinides: potentiate insulin secretion
§ Medication example: repaglinide, nateglindide (“ides” can potentiate or cause a hypoglycemic state because its increasing insulin levels)
o Glitazones: improve insulin sensitivity (fat, liver, muscle) (tricks to think the BGL level is high, and more sugars are not needed
§ Medication example: pioglitazone, rosiglitazone
o A-Glucosidase inhibitor: delay intestinal carbohydrate absorption (blocking the enzyme form ??)
§ Medication example: acarbose, miglitol
o GLP1 Receptor Agonists: potentiate insulin secretion, decrease glucose secretion, slow gastric emptying
§ Medication example: Exenatide, liraglutide
o SGLT2 Inhibitors: block glucose reabsorption by the kidney
§ Medication example: canaglifiozin, dapaglifiozin
o DPP4 Inhibitors: potentiate insulin secretion and decrease glucagon secretion (inhibiting the process of glucagon production???
o Amylin Mimetics: decrease glucagon secretion, slow gastric emptying
§ Medication example: pramlintide
Diabetic Ketoacidosis (DKA) (high levels of acidity = high levels of k+)
- It is an acute, life-threatening complication of diabetes mellitus
- DKA occurs predominantly in insulin-dependent (T1DM) patients
- DKA is a response to cellular starvation brought on by relative insulin deficiency and counter-regulatory or catabolic hormone excess
- Insulin is the only hormone produced by the pancreas and is responsible for the metabolism and storage of carbohydrates, fat and protein
- After prolonged inability to utilize glucose, cells will begin to utilize fatty acids as a source for cellular respiration
- Adipose cells break down triglyceride fats into component fatty acids, which then enter the circulation
- If not used directly by the cells, the liver will catabolize the fatty acids to acetoacetic acid
- When more of this is released by the liver than can be utilized, it accumulates along with acetone and B-hydroxibutyric acid
- These are ketone bodies, and their presence in the bloodstream is termed ketosis
- These ketones (along with the lactic acid produced from decreased tissue perfusion and as a by-product of cellular respiration without glucose) will cause a drop in pH – metabolic acidosis (and cause a hyperkalemic state)
- The increased glucose in the vasculature (hypertonic) will cause an osmotic extracellular shift
- The increased glucose in the kidneys will not be reabsorbed from the proximal tubules if systemic BGL is above 10mmol/L
- This will cause osmotic shifting into the kidneys and into the urine
- This fluid shift from the cells into the vasculature to the urine will cause profound dehydration and the arrhythmias that follow.
- Electrolytes will follow the fluid shift out of the body, the most common being (Na, K, Mg and PO4 (phosphate)
- Potassium is of particular concern because a drop in pH will cause an extracellular shift of K. This will cause an initial spike in serum K levels, but as diuresis continues, and pH is raised due to treatment (causing an intracellular shift of K) levels will drop dramatically
o The biggest problem is the cardiac arrhythmias
- Sodium is also of concern because if too much is lost by the time serum glucose levels begin to drop, cerebral edema will occur as a result of fluid therapy. (correct the blood sugar, we are hyponatremic, low sodium in the cells, need to be balance the sodium between the blood and the cells and the fluid shift can cause the cerebral edema)
Mechanism of Diabetic Ketoacidosis
What Causes DKA?
- Omission of insulin
- Dislodgement of insulin pump catheter
- Infection
- Pregnancy
- Hyperthyroidism, pheochromocytoma, Cushing syndrome
- Medications: steroids, thiazides, antipsychotics, sympathomimetics
- Heat-related illness
- Cerebrovascular incident
- GI hemorrhage
- Myocardial infarction
- Pulmonary embolism, pancreatitis, surgery major trauma
Differential Diagnosis for DKA
- Alcoholic ketoacidosis
- Starvation ketoacidosis
- Renal failure
- Lactic acidosis
- Ingestions of: salicylates, ethylene glycol, methanol
Signs and Symptoms
- Initial signs and symptoms include:
o Polydipsia, polyuria (generally only symptoms until ketonemia and acidosis develop)
- As DKA worsens and more body systems become involved, a patient will present with the following:
o Tachypnea (blow off PCO2) (kussmals respirations, fruity breath)
o Peripheral vasodilation (despite large loss of volume)
o Unexplained abdominal pain, N/V (vomiting exacerbates potassium loss); this is seen especially in children
- Further progression and worsening condition of the patient:
o Altered mental status
o Tachycardia
o Orthostatic hypotension
o Poor skin turgor
o Dry mucus membranes
o Kussmal respirations
o Fruity odour (due to acetone production in the body)
o Fever (not always present)
o Hypothermia (occasionally present due to peripheral vasodilation, not environmental temperature drop)
Assessment
- BGL
- 12-lead ECG (look for hyperkalemia)
- An ABG
- CBC (complete blood count)
- Serum electrolytes, BUN, Creatine
- Urinalysis
- Calculate the Anion Gap
DKA leads to a wide anion gap = metabolic acidosis
DKA Treatment
- Cardiac monitoring
- Establish IV 16 or 18g with isotonic crystalloid infusion
- Establish a second IV with 0.45% (hypotonic solution) normal saline TKVO (we font do this because the risk of cerebral edema is too high)
- Aggressive Fluid Therapy goal is:
o Volume repletion
o Reversal of metabolic consequences from insulin insufficiency
o Correct electrolyte and acid-base imbalance
o Recognition and treatment of precipitating causes
o Avoidance of complications (would give sodium bicarb only if hyperk is shown on the ECG)
- Treatment should follow four themes in order of precedence:
o Fluid replacement
o Electrolyte replacement
o Hyperglycemia treatment
o Acidosis treatment
- Fluid resuscitation should follow standard 20ml/kg bolus (Pt will need massive amounts of fluid). Use an antiemetic to help prevent further dehydration
- Potassium will be the only electrolyte of concern in the pre-hospital setting
- Look for ECG changes and treat based on them. In the hospital setting, KCL will be initiated when serum K levels drop below the upper range of normal. This prediction is that K levels will continue to drop as acidosis is corrected.
- Insulin therapy is continued even after BGL drops below 13.8mmol/L because it allows a gradual decrease in serum glucose levels and ketone levels
- However, a 5% dextrose infusion is begun at this point to avoid hypoglycemia. If serum Bicarb levels are available, the insulin can usually be stopped when they reach 18mEq/L (sufficient enough to combat the ketoacidosis without the insulin)
- Sodium Bicarbonate should only be used in the pre-hospital setting if there are ECG changes indicative of hyperkalemia. In the hospital setting, it is also used when measured pH and bicarb is low. Dosing is generally 50-100mEq in 1 L NS over 30-60 minutes (or 1mEq/kg)
- The goal of treatment is BGL < 11.1mmol/L, Bicarbonate level => 18mEq/L and pH >7.3
- Bicarb is dangerous to use in DKA because it is hypertonic and hyperosmolar, which will cause a further increase in intravascular volume
Hyperosmolar Hyperglycemic State (HHS)
- Progressive hyperglycemia and hyperosmolarity that is generally seen in patients who are debilitated and have poorly controlled type 2 Diabetes mellitus (T2DM)
- Generally, these patients have limited access to water and other comorbidities.
- Most commonly, this condition is seen in the elderly, but factors such as obesity and African American race are putting children at a higher risk for the development of HHS
- 3 factors make up HHS:
o Insulin resistance and/or deficiency
o An inflammatory state with elevation in pro-inflammatory cytokines and counterregulatory stress hormones that cause increased hepatic gluconeogenesis and glycogenolysis
o Osmotic diuresis followed by impaired renal excretion of glucose
Pathophysiology:
- As serum glucose levels increase, an osmotic gradient develops and causes water from the intracellular space into the intravascular compartment
- This causes cellular dehydration
- As the intravascular volume increases, the kidneys go into overdrive to eliminate the excess fluids containing glucose. (hence an increase in GFR)
- Because there is to much glucose for the kidneys to reabsorb this further causes glucosuria and osmotic diuresis to occur.
- Significant loss of sodium, potassium, calcium, phosphate and magnesium may occur during diuresis
- As volume depletion progresses à renal perfusion decreases, à kidney GFR reduced
- As the kidneys can't get rid of the glucose, this further worsens the hyperglycemia
Elderly patients develop signs and symptoms over days to weeks and complaints are nonspecific:
- Abnormal vitals signs, altered LOC
- Weakness, anorexia, fatigue
- Vomiting
- Cognitive impairment
- Previous history of uncontrolled or NYD type 2 diabetes
- Previous comorbidity (pneumonia, UIT, previous cardiac, Resp, renal, neurologic impairment)
- Medication may predispose patients (diuretics, Beta-agonists (have a direct relationship to blood sugar), antidepressants, antipsychotics, phenytoin, statins)
Treatment:
- Correct hypovolemia with normal saline or ringers
- Identify and treat the underlying cause
- Correct electrolyte abnormalities (Na, Ca, K, Mg, CL)
- Gradual correction of hyperglycemia and hyperosmolarity (insulin, potassium)
Disease Complications
- Cerebral Edema is an uncommon complication in adult patients experiencing HHS
- Osmotic demyelination syndrome (ODS)
o May occur if the osmolality changes to rapidly during the treatment of HHS
- Venous and Arterial Thromboses are commonly reported in HHS patients
- These patients should receive prophylactic anticoagulation therapy if this occurs
Unusual Conditions to Watch Out For
Diabetes Insipidus
- An uncommon disorder that causes an imbalance if fluids in the body
- This condition is often related to diabetes mellitus, but THEY ARE NOT THE SAME
- Causes
o Caused by a deficiency of ADH or a condition that blocks the effect of ADH (antidiuretic hormone). When ADH gets blocked, the result is excess urine production
- Signs and Symptoms:
o Extreme thirst
o Producing large amounts of urine
o Urinating frequently at night
o Preferring cold drinks
o Note: most adults generally produce approx. 1-2 liters of urine per day. With Diabetes Insipidus, patients can produce as much as 19 liters of urine per day
- Complications
o Patients may experience dehydration and electrolyte imbalance (sodium and potassium)
Somogyi Effect & Dawn Phenomenon
Somogyi Effect
- Occurs when a person takes too much or too little insulin before bed or when they skip a nighttime snack
- Blood sugars drop drastically overnight, making the body release hormones that work against insulin
- The result is rebound hyperglycemia
Dawn Phenomenon
- The body doesn’t release more insulin to match the early morning rise in blood sugar
- Generally, occurs between 3am to 8 am
- Prevention: eat carbs before bed, take insulin before bed, use an insulin pump overnight
Both conditions cause high blood sugar levels in the morning in people who have diabetes
Insulin
- Fun facts: Activation of B2 receptors in the pancreas promotes secretion of insulin. Activation of alpha receptors inhibits release. Insulin stimulates the cellular uptake of potassium (K)
- 7 types of insulin: 1 natural and 6 modified
- 3 of the modified are faster acting with a shorter duration than regular insulin
- 3 are slower acting with a longer duration
- All are clear except for NPH (bound to protamine)
- Two processes can be used to prolong insulin effects: add a protein or alter the molecule
- All can only be given subcutaneously except regular insulin
- Regular insulin can be given SQ, IM, IV
- Short/rapid-acting: Humalog, Novolog
- Regular acting: Humulin R, Novolin R
o 0.1units/kg/hr IV/IO
o Mix 100 units in 100mL normal saline (1unit/mL)
- Intermediate NPH) acting: Humulin N, Novolin N
- Long-acting: Lantu
Mind Map: Healthy Lifestyle
Central Idea
Healthy Lifestyle
Main Branches
1. Nutrition
Balanced Diet
Fruits and Vegetables
Whole Grains
Lean Proteins
Healthy Fats
Hydration
Water Intake
Herbal Teas
Limiting Sugary Drinks
Meal Planning
Preparing Meals in Advance
Portion Control
Mindful Eating
2. Physical Activity
Types of Exercise
Aerobic (Running, Cycling)
Strength Training (Weights, Resistance Bands)
Flexibility (Yoga, Stretching)
Daily Activity
Walking/Biking to Work
Taking the Stairs
Active Hobbies (Dancing, Sports)
Fitness Goals
Setting SMART Goals
Tracking Progress
Staying Motivated
3. Mental Well-being
Stress Management
Mindfulness and Meditation
Deep Breathing Exercises
Time Management
Social Connections
Building Relationships
Community Involvement
Support Systems
Self-Care
Hobbies and Interests
Regular Breaks
Positive Affirmations
4. Sleep Hygiene
Sleep Environment
Comfortable Bedding
Dark and Quiet Room
Cool Temperature
Sleep Routine
Consistent Sleep Schedule
Wind-down Activities
Limiting Screen Time Before Bed
Sleep Quality
Avoiding Caffeine and Heavy Meals
Relaxation Techniques
Seeking Professional Help if Needed
5. Preventive Health
Regular Check-ups
Annual Physicals
Dental Visits
Eye Exams
Vaccinations
Flu Shot
Other Recommended Vaccines
Health Education
Staying Informed about Health Issues
Understanding Family Health History
Accessing Reliable Health Resources