Complex Exam II

Serum creatinine levels

Males: 0.6-1.2

Females: 0.5-1.1

Higher creatinine levels = higher kidney damage

Blood urea nitrogen

blood test that measures the amount of urea in the blood; should be 10-20 mg/dl

AKI

Over 50% increase in serum creatinine; can be prerenal (hypoperfusion), intrarenal (physical injury such as trauma), or postrenal (obstruction of urine flow)

Acute tubular necrosis

damage to the renal tubules due to presence of toxins in the urine or to ischemia

caused by sepsis, prolonged hypotension, rhabdomyolysis

s/s: oliguria, anuria, brown urine, swelling, coma/delirium/drowsiness/confusion

dx: serum BUN and creatinine, UA, kidney biopsy

tx: treat cause, prevent fluid vol. overload and hyperkalemia

mx: fluid restriction, strict Is and Os, daily labs

normal urinary output

1000 to 2000 mL per 24 hours OR 30 ml/hr

AKI clinical manifestations

Oliguria or anuria; edema in legs/ankles/feet, fatigue, SOB, HTN, confusion, nausea, flank pain, chest pain, seizures

AKI nutrition

No more than 500-600 mL over the previous day's 24 hr UOP. Limit potassium and sodium.

AKI interventions

Avoid nephrotoxic meds, avoid hyperkalemia (kayexalate, insulin), avoid hyperphosphatemia, avoid severe metabolic acidosis, admin. diuretics

Most common causes of kidney disorders

Uncontrolled diabetes (high glucose levels damage glomeruli), uncontrolled HTN (causes hardening of renal arteries), heart disease/atherosclerosis (decreased blood flow to kidneys), obesity, smoking

Primary glomerular disease

Non-systemic damage and inflammation within the kidneys

Nephrotic syndrome

Proteinuria; increased glomerular permeability leads to protein leakage (will have low serum albumin and low serum protein)

dx: blood work for albumin, sCr/BUN/GFR, UA

mx: strict Is and Os (watch for oliguria), control BP through diuretics, ACEis etc., anticoagulant therapy since body's anticoags are dumped out into urine

Nephritic syndrome

Hematuria; inflammation of the glomeruli causes bleeding (will have high BP, oliguria, azotemia and edema)

dx: BMP (sCr will increase quickly), UA

tx: diuretics, ACEis, fluid and Na+ restrictions, abx if needed for underlying infection

Glomerulonephritis

Immune system attacks kidneys and injures glomeruli.

HAD STREP: HTN, a positive strep titer, decreased GFR, swelling in face/eyes, tea colored urine, recent strep infection, elevated BUN and sCr, proteinuria (mild)

dx: UA, CMP

mx: daily weights, watch for fluid overload

Chronic glomerulonephritis

condition in which the glomeruli suffer gradual, progressive, destructive changes, with resulting loss of kidney function; also called chronic nephritis. caused by repeat acute glomerulonephritis, HTN-related nephrosclerosis, hyperlipidemia. will have hyperkalemia, metabolic acidosis, hypoalbuminemia, anemia.

dx: UA/CMP/CBC, kidney US

mx: daily weights, high protein diet

polycystic kidney disease (PKD)

multiple fluid-filled sacs (cysts) within and on the kidney; will have hematuria, polyuria, and proteinuria; as well as HTN, renal calculi, flank pain, UTI, palpable cysts on exam

mx: no available tx so supportive mx with BP control, kidney transplant

CKD staging

G1: GFR > 90

G2: GFR = 60-89

G3a: GFR = 45-59

G3b: GFR = 30-44

G4: GFR = 15-29

G5: GFR < 15

CKD nutrition

low sodium (2-3 g a day)

low fluids

low phosphorus

increase protein only of 1.-1.5g per day when on dialysis

regulatory mechanisms in shock

pathophysiology of shock

cells switch to anaerobic metabolism, creating lactic acid; cell function ceases and swells and membranes become more permeable, with electrolytes seeping out of cells. na/k pump and mitochondria fail and cell death and lysis begins to occur.

stages of shock

Initial insult

Compensatory

Progressive

Irreversible

progressive stage of shock

when compensatory mechanisms fail and organ functions begin to deteriorate

clinical manifestations of shock (compensatory)

Tachypnea, tachycardia, diaphoresis, cool or clammy skin, decreased UOP, increased serum glucose, hypoactive bowel sounds, decreased PaCO2

clinical manifestations of shock (progressive)

hypotension (late sign), pulmonary edema w/ crackles, multiple organ dysfunction syndrome (MODS), altered mental status, AKI (oliguria, anuria), GI ischemia (bloody diarrhea, ulcers), abnormal hemostasis (increased clotting times, bruises, petechiae), tachycardia/tachypnea

multiple organ dysfunction score

signs of MODS

respiratory P/F ratio <250 w/o pneumonia, or <200 w/ pneumonia (PaO2 to FiO2 ratio)

MAP <65 mmHg; SBP <90 or SBP decreases >40 from baseline

creatinine > 2 mg/dl

urine output <0.5 mL/kg/hr in 6 hours or <400 mL in 24 hours

bilirubin > 2 mg/dl

platelets <100,000/mm3

INR > 1.5 or aPTT > 60 secs

lactate > 2 mmol/L

clinical manifestations of shock (irreversible)

significantly diminished cardiac output, pale/cyanotic/yellowish skin, anuria, disseminated intravascular coagulation (widespread clot formation, clotting factors get used up and patient develops uncontrollable bleeding)

hypovolemic shock: causes

blood loss, dehydration, burns, diarrhea/vomiting, diabetes insipidus, diuresis (such as hemodialysis)

hypovolemic shock: clinical manifestations

poor skin turgor, thirst, oliguria, low systemic and pulmonary preloads, rapid heart rates

hypovolemic shock: management

Find the source and stop it! ​

Replace lost intravascular volume​

Redistribute fluid volume

hypovolemic shock: tx

surgical intervention to control bleeding, IV fluid resuscitation (isotonic), blood transfusion (usually if Hgb < 7 g/dL)

1 unit of PRBCs should raise Hgb by what?

1 g/dL

cardiogenic shock: causes

MI (most common), HF, dysrhythmias, CAD, cardiomegaly, myocarditis, valvular disorders, drug toxicity

cardiogenic shock: clinical manifestations

crackles in lungs, chest pain, weak and thready pulses, hypoxemia, fatigue, diaphoresis

cardiogenic shock: management

restore tissue perfusion, improve cardiac contractility, manage other organ dysfunction

cardiogenic shock: tx

Thrombolytics, PCI, stents; meds (dysrhythmias, electrolyte imbalance correction), mechanical assistive devices (IABP, impella, LVAD); use fluids with extreme caution. major purpose of tx is to correct underlying cause

obstructive shock: causes

pneumothorax, cardiac tamponade, PE, aortic dissection, pulmonary hypertension, restrictive cardiomyopathy

obstructive shock: clinical manifestations

chest or abd. pain, distended jugular veins, muffled heart sounds (in cardiac tamponade), unequal peripheral pulses (in aortic dissection)

obstructive shock: management

remove the obstruction

obstructive shock: tx

Fibrinolytics and DOACs (for PE)​

Surgical intervention (for PE, tumors, aortic dissection, or

splenic sequestration)​

Needle decompression/chest tube (for pneumothorax)​

Pericardiocentesis (for cardiac tamponade)​

Medications (HTN meds for restricted cardiomyopathy or PH)​

Use fluids with extreme caution

distributive shock: causes

anaphylaxis, sepsis, spinal cord injury

distributive shock: clinical manifestations

warm or flushed skin due to widespread vasodilation (blood sits in blood vessels for longer than normal), other systems dependent on type of distributive shock

distributive shock: management

main goals are restoring sympathetic tone, reversing cause, supporting BP/pulse/respirations

distributive shock: tx

if neurogenic: spinal stabilization or surgery; atropine for parasympathetic induced bradycardia, DVT/VTE prophylaxis; if anaphylactic: IM epinephrine

distributive shock: neurogenic

interruption of sympathetic nervous system impulse transmission caused by injury to brain or spine; causes include meningitis, spinal anesthesia, stroke

*parasympathetic nervous system takes over, promoting bradycardia and worsening cardiac output

distributive shock: anaphylactic

major release of histamine leads to widespread hypotension and vasodilation

distributive shock: septic

an infection causes an exaggerated inflammatory response by the body, causing widespread vasodilation, hypotension, and organ damage

general treatment for shock

early identification (ABCs, vitals, lab trends, subtle changes including LOC, UOP, skin tone, cap refill), establishing adequate tissue perfusion (restoring intravascular volume and vasomotor tone to increase CO, adequate oxygenation), restoring normal cell function (restore acid-base balance, provide nutritional support, prevent GI injury), monitor labs (lactate levels, ABGs, signs of MODS, CMP, CBC), monitor BP and MAP, provide psychosocial support and advanced supportive care prn (ventilation, dialysis, etc.)

general fluid replacement for shock

fluid challenge (one time): 500-1000 mL bolus of isotonic fluids

aggressive fluid resuscitation (long-term): 30 mL/kg using ideal body weight of isotonic fluids

fluids used include lactated ringer's, 0.9% NS

complications of fluid replacement

if insufficient: higher incidence of morbidity and mortality due to lack of tissue perfusion

if excessive: higher incidence of morbidity/mortality due to multiple side effects, including acute lung injury, abd. compartment syndrome, MODS, hypothermia, acidosis

nutritional therapy for shock

caloric intake starts low and then increases, protein starts high and then decreases.

Narrow pulse pressures can be an indicator of shock from ______________ ______ or _______________ ________

decreased CO, increased SVR (systolic vascular resistance

MAP formula

(SBP + 2DBP)/3; normal range 70-100 mmHg

ScvO2 normal range

70-80%

PaCO2 normal range

35-45 mmHg

CVP (central venous pressure) normal range and significance

8-12 mmHg; used to estimate right atrial pressure and overall fluid status

PAP (pulmonary artery pressure) normal range and significance

12-20 mmHg mPAP; used to estimate right ventricular function and assess for pulmonary HTN

PAWP (pulmonary artery wedge pressure) normal range and significance

6-12 mmHg mPAWP; used to estimate left atrial pressure. low in hypovolemic and distributive shock, and can be either high or low in obstructive shock depending on cause

Systemic inflammatory response syndrome (SIRS)

a syndrome resulting from a clinical insult that initiates an inflammatory response that is systemic, rather than localized to the site of the insult

SIRS criteria

2 or more of the criteria must be met:

HR greater than 90

RR greater than 20

Temp greater than 100.9 or less than 96.8

WBC greater than 12,000/mm3 or less than 4000/mm3 or > 10% bands

glucose greater than 140 mg/dl in absence of diabetes

______________ levels are used to guide sepsis resuscitation efforts.

lactate

Sepsis 1 hour bundle

1. Measure lactate level. Remeasure if initial lactate elevated (>2).

2. Obtain blood cultures x2 prior to administering antibiotics.

3. Begin rapid administration of 30ml/kg crystalloid.

4. Administer broad spectrum antibiotics.

5. Administer vasopressors if needed.

persistent hypotension and vasopressor indications

B/P is measured every 15 minutes post-fluids​. Two consecutive low B/P readings indicates persistent hypotension​, and vasopressors should be started without delay.

Additional sepsis medications

volume expanders (albumin) to increase intravascular volume and improve BP; corticosteroids (hydrocortisone) to reduce inflammatory response and limit vasodilation; PPIs (pantoprazole) to protect the gut from stress ulcers or bleeding; antipyretics, insulin, etc.