Critical Care Exam 5 Dr. Smith

Plain Thrombocytopenia vs. HIT

#1 concern is bleeding Plt count < 150000 Mild: 70-15 Moderate: 20-70 Severe: <20000 Heparin-Induced Thrombocytopenia: #1 concern is clot formation Lymphocytes produce Abs that destroy PLTs 1. Incr PLT destruction (idiopathic, DIC, Lupus) 2. Decr PLT production (bone marrow suppression) 3. Splenic sequestration of plts (alcoholism) 4. Massive consumption of plts 5. PLT dilution (fld overload)

Tumor lysis syndrome

#1 problem fluid/elct balance but can be related to actual problem Ex. high K may cause decr. CO due to dysrhythmia Oncologic emergency, variety of metabolic disturbances seen with tx of CA - usually r/t chemotherapy and biologic agents and radiation in the tx of malignant disorders (lymphoma pts) ***Destruction of massive numbers of malignant cells*** → Hyperuricemia (nucleic acids metabolized into uric acid) Hyperkalemia (cell lysis release of intracellular K) (3.5-5.3) Hyperphosphatemia (cell lysis release of intracellular PO4, renal damage) Hypocalcemia (from rapid incr of phosphorous)

Heparin-induced thrombocytopenia (HIT)

#1 problem is clot formation/thrombosis/perfusion Adverse rxn to Heparin (Heparin-Ab complexes form and adhere to PLTs, PLT stimulation results in release of thrombin and PLT clumping → drop in PLTs within 5-10 days of initial exposure or immediate response if prior exposure) Type 1: non-immune mediated, transient, mild (just D/C the heparin, more common) Type 2: immune-mediated response to heparin therapy (life-threatening, less common), normally heparin should not affect plts so if plts start to drop then heparin is causing it

Acute Tubular Necrosis (ATN)

(a form of intrarenal AKI) Damage to renal tubular epithelium that px concentration of urine, filtration of wastes, and acid-base and fld/lyte balance If both BUN and Creatinine are elevated, it is a kidney issue (intrarenal) Fractional Excretion of Na (FENa) - should not have Na in urine, s/b filtered into blood < 1% suggests prerenal compromise > 2% suggests ATN (intrarenal)

Pre-renal AKI

(heart, descending aorta, renal arteries) Impaired renal blood flow from renal arteries off of descending aorta leads to decr GFR and ATN (Acute Tubular Necrosis?) Possible causes: HOTN or hypoperfusion from flds shifts from shock, burns Prolonged low CO from HF/trauma/loss Renal vasc thrombosis from clot to kidney Prolonged vascular thrombosis (V/D, bleed, Obgyn, burn, shock) Patho: decr. filtration pressure, decr. GFR, acute tubular necrosis (cortical), AKI Ischemic: severe decr. BP (vol, cardiac, vascular changes), renin production/vasoconstriction, glomerular injury/decr. glomerular permeability, decr. GFR, ischemia -> patchy cell edema, injury/necrosis ***Damage to renal tubular epithelium and vasculature, prevents concentration of urine, filtration of wastes, regulation of acid-base/elect/water balance

Intra-renal AKI

(kidneys) Ischemic perfusion injury, inflammatory, or toxic insult to nephrons (dye) resulting in cellular damage to renal vasculature/glomerulus/tubules/intersitium → leaking of proteins and reflux of cellular debris into tubules → obstrx and ATN Possible causes: Kidney ischemia (advanced pre-renal injury) Uncorrected hypoperfusion Renal artery thrombosis (sepsis, DIC, HIT, sickle cell, crush injury) Shock Endogenous toxins (rhabdo, tumor lysis syndrome) Exogenous toxins (nephrotoxic drugs/dyes, pesticides, transf rxn/nephrotoxic drugs) Infection (acute glomerularneprhitis and interstitial nephritis) Obstructive: thrombosis/sickle cell/trauma/crush injuries from rhabdomylosis Patho: Nephrotoxic - nephrotoxic agent = substance that has a destructive effect on renal cells + multiple pre-existing factors (DM, dehydration, age, renal insufficiency), concentrate in medulla, nephron necrosis in proximal tubule

Idiopathic thrombocytopenia purpura

(rash of purple spots, autoimmune) Patho: lymphocytes produce antibodies that destroy existing plts S/sx: Petechial hemorrhages, bruising, unusual bleeding PLTs < 30,000 but normal coag studies and clotting times Tx: May resolve spontaneously Adm. glucocorticoids (suppress the immune system), PLTs, or IV immunoglobulins (IgG Ab), steroids Prep for splenectomy if sequestration Nsg mgmt: prevent bleeding, use bleeding precautions

Post-renal AKI

(ureters, bladder) Urinary tract obstrx that affects kidneys bilat Possible causes: Bladder outlet obstrx Prostatic hypertrophy Bilat ureteral obstrx Edema (after cath of ureter, pressure goes upstream and causes decr. GFR)

Phases of AKI ONSET

- period from initial insult until cell injury occurs - ischemic injury evolving - decr. renal blood flow - decr. GF pressure - interrupted tubular epithelium (damage) - lasts hours to days - reversible (replace volume and restore perfusion pressures)

Hemostasis

1. local vasoconstrict to reduce blood flow 2. plt aggregation and formation of a plt plug 3. form a fibrin mesh to strength the plug 4. clot dissolution after tissue repair is complete

Magnesium

1.5 - 2.5 mEq/L H: CNS and resp depression, bradycardia, lethargy, coma (calm & quiet) L: cardiac dysrhythmias, facial tics, spasticity (buck wild)

Sodium

135 - 145 mEq/L H: extreme thirst, altered mentation, possible seizures L: disorientation, muscle twitching, N/V/cramps, HA, dizziness, cold/clammy, tachycardia, oliguria, possible cerebral edema Tx: Dilutional hyponatremia corrected with fld restriction or dialysis bath

Phosphorus

2.7 - 4.5 mg/dl H: tachycardia, diarrhea, muscle weakness, incr reflexes (mimics low calcium) L: anemias, decr WBC fxn, bleeding, N/V, anorexia (mimics high calcium) Tx: high phos foods (nuts, dairy, processed foods, brown sodas)

Phases of AKI RECOVERY

3-12 months 30% do not have full recovery Cr decreases as renal fxn improves

Potassium

3.5 - 4.5 mEq/L H: anxiety, N/V/D, incr r/f coding (tight and contracted) Tx: Lasix, D50Insulin, Kayexalate, Dialysis L: abd distention, paresthesia, decr reflexes, confusion, dizziness, Dig. toxicity, alkalosis, shallow resp, thready pulse (low and slow)

Calcium

8.5 - 10.5 mg/dl H: excessive thirst, anorexia, deep bone pain, lethargy, weakened muscles (swollen & slow with moans, groans, and stones) L: muscle cramps/tetany, decr CO, bleeding, pos Chvostek or Trousseau, tingling of mouth/fingers (Mexican dance moves) Tx: Cal and Vit D supplements, dietary phos binders (PhosLO)

Chloride

98 - 108 mEq/L (mimics high and low sodium) H: weakness, lethargy, deep/rapid RR, possible unconsciousness (big and bloated) L: hyperirritability, tetany, slow RR, fever (depressed and deflated)

Primary assessment of emergent care is performed

A (maintain patent airway, tongue) B (ensure ventilation, chest tube) C (circulation/c-spine) Cervical spine immobilization Disability (neuro, alert/verb/pain/unresp, eyes) Decontamination Exposure (keep them warm, acidosis, O2 consumption with shiver, clotting, alcohol dilates, hypothermia shift to left oxyhema curve) Fld vol replacement begin Hypovolemic shock most common: Multiple large bore lines, rapid infusers (and maybe a Cordis introducer) Crystalloids (LR) then colloids (plasma, albumin, or blood products), fld warmers 1) Follow the primary survey 2) then a treatment decision is made 3) then fully assess victim

Hypokalemia (What will you see?)

A SIC WALT Alkalosis Shallow respiration Irritability Confusion and drowsiness Weakness and fatigue Arrhythmias- irregular heart rate, tachycardia Lethargy Thready pulse decrease intestinal mobility, nausea and vomiting EKG: flattened/inverted T wave, prominent U wave, ST depression, QT prolongation

Portal HTN

Abnormally high BP in portal venous system (this is usually a low pressure system) Causes: disorders that obstruct blood flow through portal system or vena cava; thrombosis, inflammation, fibrosis of sinusoids (cirrhosis, viral hep, or schistosomiasis), R sided HF (backup), constrictive pericarditis Patho: inc portal vein BP → collateral vessels dilate to lower pressure → blood bypasses the obstructed portal vessels (path of least resistance) → collateral veins develop in lower esophagus, anterior abd wall, and rectum (See visible veins) → inc pressure and inc blood flow transferred from portal venous system to systemic venous circulation (begins to worsen)

Metabolic abnormalities

Acid base Metabolic acidosis d/t inc lactate/renal failure Respiratory acidosis compromise from abd distention or dec RR Respiratory alkalosis= inc RR from hepatic encephalopathy Hypoglycemia: inc intitally d/t stress, then d/t dec gluconeogenesis Treatment: freq glucose checks, IV 10% dextrose, IV D50 prn, remember normal carb is affected Electrolytes: dec Mg, dec phosphorous, dec K d/t diuretics and poor intake; dec Na usually dilutional, correct slowly Inflammatory response: decr. MAP, decr. SVR (vasodilate), decr. Preload = fluid shifts Treatment: correct underlying problem, Na bicarb if needed

Management of TLS

Adequate hydration, correct metabolic imbalances, monitor lytes and ABGs, prevent complications - lower K+ by giving insulin and D5, kayexalate gets rid of it quickly, lasix, dialysis, GIK (glucose/insulin/K) - antacids to tx hyperphosphatemia - stool softeners - calcium gluconate to replace calcium - Diet restrix of K and Phos - Adm. NaHCO3 to incr pH to incr solubility of uric acid Adm. Allopurinol to decr production of uric acid - frequent phlebotomy, coagulopathies, nutritional deficits

Liver labs

Alkaline phosphatase = 40 - 140 units/L (our lab sheet says 38-126 U/L) AST/SGOT = 10-30 U/L ALT/SGPT = 10-40 U/L Bilirubin: Total 0.2-1.3 mg/dL Direct: 0.0-0.4 mg/dL

Baroreceptors/neural in renal regulation

Baroreceptors in carotid and aortic arch stimulate vasoconstriction - renal blood vessels innervated by ANS causing vasoconstriciton - signals from Carotid sinus and baroreceptors in aortic arch stimulate vasoconstriction

Abd injury

C/b from gunshot wounds, stab wounds, seat belt injuries, any abdominal trauma S/sx: Cullen's sign (umbilical ecchymoses, abd bleed), Grey Turner sign (flank ecchymosis, back bleed, pancreas damage), Kehr sign (left shoulder pain, spleen, bleed irritates phrenic nerve referred pain) Peritoneal bleeding signs: guarding, abdominal pain, rigidity Hx: restrained, pain, N/V, need to eliminate Exam: contour, seat belt mark, GSWSW, peritoneal signs Dx: foley, NGT, Hgb, CT, abd films, IVP, FAST (US), occult blood, HCG, DPL (lavage diagnostic test)

Ascites mangament

Caused by inc pressure in portal vein Hydrostatic pressure forces water out of vessels and into the peritoneal cavity Causes: Cirrhosis, HF, constrictive pericarditis, abdominal malignancies, nephrotic syndrome, malnutrition (lack of albumin causes fluid shift) Contributing factors Inc NA retention by kidneys, inc lymph production, inc portal pressure, dec capillary osmotic pressure (dec albumin from leaking), inc aldosterone and ADH s/s: wt gain, abd distention (incr. pressure and diaphragm can't expand), inc abd girth, dyspnea, inc RR, orthopnea, peripheral edema Complications: peritonitis : fever, chills, abd pain, dec bowel sounds, cloudy ascitic fluid fluid shift: hypotension and fluid/elect. imbalance Treatment: Paracentesis (only remove couple L at a time or cx hypotension/shock) Dec Na diet Diuretics (don't take off more than a few liters at a time to px complications of rapid fluid shift) Surgical intervention: TIPS, liver transplant, shunt - if portal HTN and ascites = poor prognosis

Hormonal regulation

Cells that surround the Afferent arteriole (juxtaglomerular apparatus) secrete renin (activating RAAS and ADH systems, sodium and water retention to maintain pressure) Renin-angiotensin system - ADH = regulates final urine concentration - Aldosterone = promotes Na+ and H2O retention

Hem/onc

Coagulation mechanism (clotting factors and pathways) stimulated by damage to endothelium (i.e. sepsis, shock, burns, DM)

Renal injury (Labs)

Creatinine = 0.5 - 1.2 mg/dl BUN = 5 - 20 mg/dl BUN:Cr = 10:1 GFR = > 90 ml/min (> 60 is ok) Albumin = 3.5-5 H/H (M,F) = 13.5-17.5, 12-16/40-54%, 37-47% SpGr = 1.005-1.025 Na = 135-145 K = 3.5-4.5 Cl = 98-108 Ca 8.5-10.5 Ph 2.7-4.5 Mg 1.5-2.5 Bicarb 24-28

Coagulopathies

Dec clot formation d/t dec synthesis of clotting factors Dec absorption and utilization of vitamin K Inc clot breakdown Dec production of antithrombotics Dec absorption and utilization of vitamin K GI bleeding uses clotting factors up Treatment Prevention, RBCs (low H/H), PLTs (< 50,000 with active blood loss or before invasive procedure; < 10,000 even without active bleed), Vit K (takes a couple of days to actively produce), FFP (if INR > 1.5 with bleeding or a invasive procedures, works quicker than Vit K), cryoprecipitate if fibrinogen < 100 GI bleeding: treatment depends on location of bleed. Prophylaxis includes PPI or H2 inhibitor, invasive procedures, platelets administration d/t bleeding from varices

Liver dysfunction #1 nsg dx

Depends on underlying cause - fluid/electrolyte - cerebral edema - respiratory - infection - CO

Hyperphosphatemia (what will you see?)

Dialysis, phosphate binders; muscle cramps, tetany, dysrhythmias, seizures

DIC

Disseminated Intravascular Coagulation (DIC) - consumptive coagulopathy - bleeding/thrombosis, depleted clotting factors, plt, RBCs, MODS, death - etiology: sepsis, massive trauma/burns (tissue factor), obstetric emergencies (placenta) - widespread micro thrombi, activate plasmin and fibrinolysis - Complication of other serious life-threatening conditions (i.e. sepsis, massive trauma or burns, obstetric emergencies) damage to endothelium and activation of coagulation mechanism → uncontrolled bleeding, depletion of clotting factors, PLTs, and RBCs → simultaneous bleeding and thrombosis (look for measures of FDP and d-dimer, if elevated there has been a lot of clot formation, really high levels prevent proper clotting) - S/S: cyanosis, gangrene, #1 NANDA: Fluid Deficit r/t active bleeding then decr tissue perfus r/t clot formation, decr CO r/t altered preload (if not active bleeding), r/f infection, anxiety, compromised family coping

Hepatic Encephalopathy

Disturbance in CNS function resulting from hepatic insufficiency; interruption of nerve impulse transmissions and causes cognitive and behavioral changes Worsened by medications, infection, bleeding, fluid/lyte imbalance, hypoxia Inability of liver to convert ammonia to urea (version that can be excreted) → toxins circulate to brain (NH4 = most dangerous from protein breakdown) → alters cerebral energy metabolism; interferes with neurotransmitters Causes inc ICP (cerebral edema/herniation) - herniation = shift of brain tissue from one side to another, down into foramen magnum -> pressure on cerebral vessels -> death S/S Early: Personality changes, memory loss, irritability, lethargy, sleep disturbances Late: confusion, asterixis (flapping wrists), stupor, convulsions/ seizures, coma → death Treatment: Dec NH4- admin lactulose which px absorption of NH4 in colon this is PO or NG tube; give neomycin to dec bacterial action in the colon/on feces Correct fluid/lyte imbalance Restrict dietary protein (esp. with renal failure) Zinc replacement- thought to inc clearance of NH4 Short acting sedation only- many sedatives metabolized in the liver, so it will act on the patient longer d/t dec liver function Nursing care: ***#1 nsg dx = der. intercranial adaptive capacity r/t cerebral edema*** Pt safety Prevention of aspiration Assessment of changes Nutritional care Education- mainly the family members

HIT mgmt

Early ID (evaluate baseline PLTs before initiating Heparin tx, Ns job) ***Obtain baseline plt count before starting heparin*** D/C Heparin as soon as PLT count falls significantly Adm. Argatroban (direct thrombin inhibitor / anticoagulant infusion $$$) Monitor for S/S HIT, ensure all types of heparin D/C and indicate them as "allergy", provide comfort/emo support, pt education Monitor for complications (DVT, PE, acute limb ischemia, ischemic stroke, AMI)

Secondary assessment

Fahrenheit / Family Gadgets to monitor and tx (i.e. V/S monitoring, lab work, pulse ox, foley, NGT/OGT, invasive lines) History / Head-to-toe assessment (AMPLE) Allergies Medications Past hx / Pregnancy Last meal Events/Environment of injury Inspect all over patient, posterior aspect Distracting injuries, family issues, extrication time

Clot breakdown

Fibrinolysis begins when fibrin clot forms (plasminogen precursor to plasmin binds to fibrin and the injured epithelial wall releases TPA which converts plasminogen to plasmin). Plasmin digests fibrin; fibrin degradation products (FDP) and d-dimer act as anticoagulants to px further clots.

Bleeding Precautions and Injury Prevention (p. 909)

Gentle with ambulation and draw sheets, fall precautions Instruct pt/family to notify if bleeding, bruising, or trauma occur Avoid rectal temps, enemas, suppositories (lubricate liberally if suppository needed) Avoid IM injections and venipunctures (if necessary, use small-gauge needle and apply firm pressure to puncture sites for 10 mins or until site no longer oozes blood) Observe IV sites every few hours for bleeding Avoid use of manual or automatic BP cuff (remove cuff when done) Electric razor use only, soft bristle toothbrush, test urine and stool for occult blood

Acute Kidney Injury (AKI)

Glomerulus (taft of capillaries) is in the Bowman's capsule The glomerulus filters plasma (GFR is directly r/t perfusion pressure of glomerular capillaries/MAP, filtration of plasma per unit of time) Abrupt decline in renal fxn within 48 hrs Serum creatinine > 0.3 mg/dl from the high (so 1.5 mg/dl) Serum creatinine incr > 50% of baseline Baseline may be 0.6 and a value of 1.2 may look normal but that's 1.5x baseline U.O. may be normal initially but later may be oliguric (< 30 ml/hr or < 400 ml/day)

AKI management

Hemodynamic monitoring (differentiates fld overload from fld imbalance) May be intravascularly dry even though edematous bc third spacing If preload is high, then fld overload Edema from: Retention (RAAS/ADH), decr albumin (lost in urine), incr cap perm from inflamm Monitor daily wt (1 kg represents 1 L) and electrolyte balance K+: EKG changes Tx: loop diuretics, D50 and insulin, kayexalate (PO/NG/Enema), dialysis, limit K+ intake Na+: decr. due to dilution, corrected with fluid restriction, sodium levels in dialysis bath Nutrition (low protein, high carb diet, low Na/K/phos, restrict fluids), px (Mucomyst can help protect kidneys from dyes) Dialysis 3x / week allows incr in BUN, Creatinine, electrolytes & flds b/w tx May result in HOTN CRRT - continuous and gentle without significant fld shifts while correcting lytes, better for hemodynamically unstable pts, Temporary access and anticoagulation to px clots that impair flow through dialyzer Dialysis: mgmt 3x per week, relatively inexpensive, short duration, allows incr. in BUN/Cr/electrolytes/fluids btw tx, may result in hypotension, temporary access, anticoagulation CVVH: continuous therapy 12 hrs to several days, slower fluid removal rate, ultrafiltrate for those hemounstable and can't tolerate normal dialysis, removal of solute and electrolytes - cont. dialysis pt must have anticoag, maintain fluid balance, hypothermia, air emboli, minimize blood loss; labs drawn Q8H, prevent hypotension Prevention!!!, fluid resuscitation, fluid restrict, pharm mgmt, fluid removal, anemia, aceytlcystine to prevent renal problems from dye *See labs for ways to treat abnormal values*

Labs in DIC

Incr. coag: Incr PT (> 13 sec), INR (thin), PTT incr., incr in FDP (> 40 mcg/dl), D-Dimer (> 250 mcg/dl) Incr. fibrinolysis: Decr fibrinogen (< 100 mg/dl) PLTs initially normal but eventually decr (< 50,000) Impaired reg fxn: Decr in antithrombin III and protein C (factors that px PLT aggregation and clot formation) End-organ failure: resp. failure, ATN, bowel infarct, CVA

Clot formation

Injury destruct basement membrane: endothelium releases endothelin (vasoconstrict), extracellular matrix exposed, vWF brings more plt, platelet adhesion, ADP recruits more plt, TXA2 cx plt to clump, fragile hemostatic plug, tissue factor, thrombin activation, fibrin net, strong clot Extrinsic: outside injury; tissue factor & factor III Intrinsic: contact activation from damage to endothelium (sepsis); factors XII, XI, IX, VIII Pathways converge and factor X (heparin acts here) converts prothrombin to thrombin, which converts fibrinogen to fibrin, to form clot. Thrombin's arrival to the site of injury calls PLTs to site, and PLT degranulation: ADP (adenosine diphosphate recruits more PLTs, affected by Plavix) TXA (thromboxane causes PLT clumping, affected by Aspirin)

Physical hemorrhage or thrombosis

Integument: bruising, bleeding from puncture sites OR cyanosis/gangrene Cardiopulm: tachycardia, HOTN, hemoptysis, pink sputum/frank blood out of ET tube OR angina, MI, SOB, PE/chest pain, dysrhythmias, ST elevation, resp. failure (ABGs hypoxic, resp. alk) Renal: hematuria OR ATN and decr u.o., acute renal failure (BUN & Cr elevated) GI: melena, bright red blood, blood in vomit, decr bowel sounds, GI bleed OR decr/absent bowel sounds, necrosis, sepsis, ischemic bowel, abd pain, diarrhea, distended/bloated, infarct of bowel (Liver enzymes elevated) Neuro: SAH, midline shifts from incr ICP, changes in LOC/PERRLA OR thrombotic CVA, ischemic stroke

Phases of AKI DIURETIC

Last average 2 wks - increased GFR - tubular obstruction passed by edema and scarring present - can eliminate fluids but not solutes - BUN and Cr continue to elevate - UO begins to incr. 2-4 L/day - hypokalemia - hyponatremia

Autoregulation of renal system

Local mechanism based on stretch on afferent arteriolar wall, cx vasoconstriction and dilation to maintain constant blood flow, tubuloglomerular feedback = based on flow rate & NaCl concentration - If MAP decr <80, then Afferent arteriole DILATES (to incr blood flow to the glomerulus) and Efferent arteriole CONSTRICTS (to incr the pressure in the glomerulus) in an attempt to keep perfusion to the glomerulus constant Bowman's space pressure is usually low, increased pressure resists fluid & solute movement into space, may be caused by debris, decreased UO High pressures will impair filtration through glomerulus to tubules and Hypoperfusion, even if brief episode, may → AKI from damage done SBP > 180 or < 80 will lead to impaired autoregulation

Cerebral edema

Most serious complication of liver dysfunction Results in inc ICP or herniation Dec cerebral perfusion : Breakdown of blood-brain barrier → edema of astrocytes → loss of autoregulation of blood flow (altered perfusion and not able to regulate blood flow = decr. cerebral perfusion) Treatment: HOB elevated, head midline (to promote drainage and facilitate cerebral venous return) Quiet, non stimulating environment Mannitol- to dec edema, pulls fluids out of cells (osmotic diuretic with particles that draw fluid out of edematous cerebral cells, incr. UO, watch fluid/lyte balance, draw out with filter needle b/c crystallize) Hyperventilation- to dec blood flow to the brain, need adequate but not too much (ventilator) Seizure prevention Paralysis and sedation - d/t inc ICP (decr. O2 consumption) Hypothermia- to dec brain metabolism

Acute liver failure (ALF)

Occurrence of jaundice and any degree of alt mental status in a pt without preexisting liver dz who has had an illness of less than 26 weeks (jaundice precedes mental changes or hepatic encephalopathy -> coma) Clinical syndrome caused by massive hepatic necrosis → hepatic failure High mortality and morbidity rate, *most common cause is acetaminophen toxicity* Pathophysiologic changes: Impaired bilirubin conjugation → jaundice Dec production of clotting factors → coagulopathies Dec glucose synthesis → hypoglycemia Dec lactate clearance → metabolic acidosis Hypoalbuminemia (decr. oncotic pressure and leak fluid), fluid/lyte imbalances, acute portal HTN → ascites Inability to detox substances in blood, metabolic and lyte disturbances → hepatic encephalopathy S/S HA, hyperventilation (compensate for acidosis), jaundice, changing mental status, palmar erythema, spider nevi (coaguopathy), bruises, edema, asterixis (flapping of the wrist) Diagnostic Inc: AST, bilirubin, ALT, ammonia (NH4), PT/INR, fibrin and FDP Dec: glucose, potassium, sodium, platelets, fibrinogen Metabolic acidosis and/or respiratory alkalosis - PT and fibrinogen exclusively made by liver Treatment: symptoms; no cure try to support and prevent multiple organ involvement, minimize complications

Acute Tubular Necrosis (ATN) phases

Onset (from initial insult until cell injury occurs) Can't catch anything in this phase but if you know that an insult episode occurred, you can anticipate tx Onset lasts hours to days and is reversible Oliguric / Anuric Begins within 48 hrs of insult, may or may not see decr in u.o. 5-8 days non-oliguric 10-16 days oliguric Incr: BUN, Creatinine, K, Phosphorous (decr: Calcium) Metabolic acidosis (low HCO3 & pH from accumulation of waste products), edema, CHF, N/V, fatigue, incr r/f infection Diuretic Lasts 2 wks (incr GFR, tubular obstx passed but edema & scarring remain) Incr: BUN, Creatinine, u.o. incr to 2-4 L/day (normal is more like 1 L/day) Decr: K, Na (cannot concentrate flds) Recovery Lasts 3-4 months (teaching that d/c from hospital doesn't mean it's fixed, and about one-third of ppl don't return to full renal fxn) Creatinine decr as renal fxn improves

Hematology labs

PT = 10 - 13 (11-16) sec INR = 1.0 normally; 2 - 3 if taking anticoags (1.5 is thicker and 3.5 is thinner) PTT = 25-35 sec PLTs = 150,000 - 450,000 Fibrinogen = 200 - 400 mg/dl Fibrin degradation products = 2 - 10 mcg/dl D-Dimer = > 250 mcg/L is noted in DIC Hgb = 12 - 18 g/dl HCT = has gender variations but generally 40 - 50 % pp. 903-904 https://www.youtube.com/watch?v=R8JMfbYW2p4

Hospital-acquired anemia

Possible etiology: frequent phlebotomy, coagulopathy, nutritional deficits, large blood transfusions, circulatory overload, transmission of infections, immunosuppression (incr. pneumonia/surgical site infection), stored blood (incr. release of K and bilirubin), clinical RF (hemolytic rxn-> decr. O2 carrying capacity, some bind with Ca and cx hypocalcemia) Blood conservation strategies: Manage O2 delivery and consumption, adm iron and Epogen/EPO (stimulate production of RBCs), minimize blood loss, safer transfusions/alternative agents (aminocaporic acid or antifibrinolytic agents/desmopressin to stabilize clots and minimize bleeding) Autologous blood donation / autotransfusion blood collected in surg, PLT sequestration (donate own PLT), blood salvaging (autotransfuse), anesthesia-induced HOTN (decr bleeding surg to keep MAP but BP low normal to minimize bleeding), surgical techniques/instruments

Medical management of DIC (in addition to assessment)

Prevention! Maintain organ perfusion (prevent multi-organ dysfunction syndrome) - IV fluids, inotropic agents - blood transfusion of RBCs (low H/H) - Plt transfusion if needed (plt low) - Cryoprecipitate (Fibrinogen low) - FFP (clotting factors low, prolonged PT not PTT) Hypercoaguability: - anti-thrombin III ($$$, prevent clot formation), aminocaporic acid (inhibits clot breakdown, stabilizes clots) Medical Mgmt: - slow consumption of coagulation factors = heparin therapy (LVWH) & anti-thrombin III Nsg Mgmt: - frequent assessments of neuro, renal, cardiopulm, skin integrity - recognize and support vital physiologic fxn - monitor for bleeding, bleeding precautions, collab mgmt, comfort support Summary: ID/eliminate underlying cause, provide hemodynamic support to maintain organ perfus IV flds, pos. inotropes, FFP, PLTs, cryoprecipitate (contains fibrinogen), antithrombin III (px clot formation), aminocaproic acid (stabilizes clots and px breakdown), heparin (slows clotting factor consumption), initiate bleeding precautions, comfort support Thrombocytopenia - PLTs < 140,000

Liver functions

Produces bile (bile salts, cholesterol, bilirubin, electrolytes, water) necessary for digestion of fats Altered fxn → malabsorption of fat and fat soluble vitamins Bile composition: alkaline yellow/green liquid in color; made of bile salts (required for intestinal absorption of fat; 20% lost in feces, conjugated bile acids), cholesterol, bilirubin, electrolytes, water Filters the blood and removes bct (kupffer cells) and particulate matter; elimination of bilirubin Bilirubin is a byproduct of the destruction of aged RBCs Altered fxn → inc exposure to colon bacteria; inc bilirubin and jaundice Inc unconjugated bilirubin= liver dysfunction Inc conjugated bilirubin= biliary tract obstruction Metabolism of drugs, steroid hormones (sex hormones, cortisol, aldosterone), CHO, fats, and proteins CHO- stores glycogen and synthesizes glucose - receives nutrients absorbed from the small intestine & metabolizes or synthesizes them into forms that can be used by cells Fat metabolism- forms lipoproteins (cell membrane formation), converts carbs and proteins to fat; synthesis, recycling and elimination of cholesterol (needed for bile, steroid hormones, and cell membranes); formation of ketones from fatty acids Protein metabolism- deamination of proteins (removal of ammonia molecule), formation of urea from ammonia, synthesis of plasma proteins (albumin), synthesis of clotting factors (Vit K clotting factors -> elevated PT and decreased fibrinogen -> incr. RF bleeding) Altered fxn → dec drug metabolism, hypoglycemia, altered cholesterol levels, elevated blood ammonia (NH4) levels, dec albumin level (which causes edema), dec clotting factors (bleeding), disturbances in gonadal function (gynecomastia), signs of inc cortisol levels (cushings), signs of hyperaldosteronism (sodium retention and hypokalemia) - albumin transports drug so with lower albumin levels, there is more free drug in the blood and risk for toxicity (must adjust drug level for someone with liver problems) Storage of minerals and vitamins Altered fxn → deficiencies of (primarily) fat soluble vitamins - Vit K, E, A, D, B12 - Elimination of bilirubin (part of RBC breakdown) Overall: Met acidosis, incr. ammonia, hypoglycemia

What proteins prevent clot formation?

Protein C and protein S and anti-thrombin III (heparin potentiates anti-thrombin III and prevents clotting, may need to give them a dose of anti-thrombin III if heparin is not helping) - inhibit thrombin, regulatory mechanisms

Thoracic Trauma (most is r/t blunt chest wall trauma)

Pulmonary injury Simple - air in pleural space Open - "sucking" chest wound, CREPITUS (air into pleural space -> pneumo -> tension) Flail chest/pneumo: ineffective breathing pattern Hemothorax: deficit fluid vol, decr. CO Tension - air can't escape and compresses thoracic organs S/sx: dyspnea, tachypnea, tachycardia, JVD, decr/absent breath sounds, asym. Chest Tx: chest tube, vaseline gauze x3 sides, if tension pneumo suspected, 18g needle 2 ICS at MCL (can remove plunger of the syringe and place a glove on top so air can escape but won't go in) DO NOT WAIT FOR CXR (#1 Decr. CO due to pressure on heart) Hemothorax - blood in pleural cavity (can cause shift and impair cardiac fxn) S/sx: dyspnea, tachypnea, tachycardia, shock, NO JVD Tx: chest tube, thoracotomy (>1500ml or >200ml/hr autotransf. if no abd injuries)

Orthopedic injury

Rarely life-threatening but have associated injury (blood loss, neuro damage, fat emboli with long bone injury: takes 12-72 hours before you see signs of this emboli after initial injury) Six P's of frx: Pain Pulses Pallor Paresthesia Paralysis Point tenderness

Hepatorenal syndrome

Renal failure in the presence of liver failure with the absence of renal pathology; it is d/t dec blood flow to the kidneys d/t liver dysfunction - abn renal fxn, splanchnic arterial vasodilation, alterations in renal blood flow (incr. BUN/Cr and decr. UO) Diagnosis: fluid resuscitated with adequate MAP, no s/s of renal disease, sepsis, or use of nephrotoxic drugs (basically r/o all other causes of renal dysfunction) Dec GFR, dec urine sodium, inc BUN and Cr, oliguria or anuria Treatment: dialysis or CRRT, redirect internal and external renal blood flow midodrine= peripheral vasoconstrictor (alpha agonist) octreotide= splanchnic vasoconstriction albumin= oncotic agent (to dec fluid shift) At inc RF infection d/t loss of Kupffer cell function, these cells phagocytize gram-neg bacteria leaked from gut, contributing factors to compromised immune system also include malnutrition and incr. in toxins

Hyperuricemia (what will you see?)

Renal failure, uric acid nephropathy, metallic taste

Acute liver dysfunction

Results from- Primary disease process in absence of preexisting liver disease; complication of liver dz, association with MODS Etiology: shock, virulent viral infection, hepatotoxins, SIRS/MODS Shock- d/t dec perfusion/hypotension which causes ischemic hepatitis-> incr. hepatic capillary permeability, fluid shift into hepatic tissue, microthrombi develop, blockages cx further ischemia and necrosis Viral- hepatitis A & B, herpes simplex, varicella zoster (shingles) Hepatotoxins- acetaminophen (overdose w/ alcohol), industrial substances, meds (ex: rifampin, tetracycline, valproic acid, MAOIs, psych meds) SIRS/MODS- kupffer cells attack, inc hepatic permeability, organ edema and microthrombi, damage to hepatocytes, blockage of bile flow, destruction of liver tissue

Genitourinary injury

S/sx: perineal ecchymosis, bleeding from meatus/vagina/rectum, mobile prostate (NO Foley → possible permanent dysfxn), pelvic instability (don't assess this if there is obvious pelvic frx)

Hemodynamics

SIRS response- dec MAP, SVR, and preload

Trauma screening

Screen for alcohol or violence CAGE screening incr. index of suspicion for abuse/violence

Reversible causes of pulseless electrical activity (PEA)***

See Chart!

Other complications with trauma

Sepsis Fat emboli, DVT Compartment syndrome MODS (resp, renal failure, etc.) DIC Infection, respiratory failure, renal failure (see picture)

AKI causes

Severe HOTN Vascular obstrx Severe glomerular dz Other clinical conditions

Trauma units/system

System: organized system within a given region including prehospital care, acute hospital care, and rehab Level 1: these facilities are regional centers that provide leadership and total care, prevention to rehab, comprehensive care; take more complex patients (24/7 care) Level 2: expected to provide initial definitive trauma care regardless of severity of injury Level 3: prompt assessment, resuscitation, emergency operations, and stabilize, transfer to level 1 or 2; serve areas without immediate access to level 1/2

Cardiac injury

Tamponade - blood in pericardial sac (fibrous, non-elastic) → decr ventric filling (Beck's triad see pic): JVD, muffled heart sounds, decr. SBP S/sx: penetrating chest wounds, narrow pulse pressure, shock Tx: pericardiocentesis (HOB 45°, insert needle sub-xiphoid and aim toward nipple, aspirate blood, close stop-cock on syringe and attach new syringe, and if blood doesn't clot then needle is in the pericardium), possible thoracotomy Myocardial contusion S/sx: may mimic MI if large enough, dysrhythmias, chest pain Tx: monitoring of cardiac enzymes and rhythm Aortic injury S/sx: wide mediastinum, severe shock, HOTN Most will die before reaching the hospital

Normal liver

The hepatic artery brings oxygenated blood to the liver (high pressure). The liver receives 25% of the heart's CO The portal vein brings deoxygenated blood which is about 80% of the blood in the liver, and it contains absorbed nutrients from the GI system for the liver to filter (low pressure, incr. pressure w/ portal HTN mix with arterial blood -> varices) - blood flow needs to pass through liver unimpeded, with cirrhosis it impedes blood flow/incr. pressure - decr. O2 and nutrients from GI into inferior vena cava Terms to know: Glisson capsule: connective tissue around the liver. Includes blood vessels, lymph, nerves, and if it is diseased or edematous it is very painful to the pt. They will ooze lymph into the peritoneum (ascites) Hepatocytes: cells which produce bile; aka "liver plates"; are the functional liver cells Sinusoids: small capillaries between the plates of the liver cells. Have a mix of oxygenated and deoxygenated blood. Lined with Kupffer cells. Kupffer cells: phagocytes which remove foreign bacteria or organisms in the blood Bile canaliculi: small bile channels throughout the liver which drain into the common bile duct Common bile duct: large channel for bile Major duodenal papilla (sphincter of Oddi): empties bile into the duodenum and prevents backflow into gallbladder Lymphatic spaces: between liver cells where lymph drains into

HIT assessment

Thrombotic events (MI, CVA, amputation, knee replacement): plt count expected to be lower after surgery but must monitor over time, less likely to form in LMWH!!!, higher risk in women/surgical pts/CV/Ortho) Decr PLTs < 150,000 or < 50% of baseline Functional assays (HIT Abs in blood → document Heparin allergy) - Thrombocytopenia r/t heparin-antibody complexes - First exposure to heparin = plts drop 5d-2w - Second exposure to heparin = rxn within hrs b/c preformed antibodies

Types of trauma

Trauma occurs as a result of external forces - blunt: MVC, falls, assault, sports Patterned injuries: - reflect ID of wounding object or provide info about the nature of the weapon

Varices mangement

Typically lower esophageal, upper stomach, rectum; thin walled and can burst and bleed out Bleeding from esophageal varices, slow chronic bleed (anemia, melana) Treatment No effective cure Beta blockers can dec BP Stop the bleeding Sengstaken-blakemore tube (rarely used now)- like an NG but with inflatable balloons which will press along the esophagus and stomach lining to stop any varices from bleeding Octreotide- typically with vasopressin which constricts vessels to dec bleeding Endoscopic variceal ligation- sclerose the vessels or band the vessels Sclerosing agent- caustic material introduced to the bleeding varacie to scar the area and stop the bleeding TIPS procedure- bypassing the portal vein surgically; adding a shunt to avoid the sclerotic area

Assessment in tumor lysis

Unexplained wt gain (r/t fld retention bc dehydrated) Hyperactive deep tendon reflexes (incr Phos, hyperK, hypoCalc) Positive Chvostek (light tapping over facial nerve → twitching) and Trousseau (BP cuff) Diarrhea, lethargy, muscle cramps, N/V, paresthesia, weakness (d/t lyte imbalances) Incr BUN and Creatinine (uric acid nephropathy), metabolic acidosis (crystalization in kidneys leading to acid/base imbalance) ECG - flat or absent p waves, peaked or inverted T waves, widened QRS

Complications of portal HTN

Varices- distended, torturous, collateral veins (very fragile that rupture and bleed, usually CHRONIC not acute) Splenomegaly- inc pressure in splenic vein which branches from the portal vein Ascites- accumulation of fluid in the peritoneal cavity (not usually compartment syndrome because gradual over time)

Hyperkalemia (what will you see?)

Vent dysrythmias, weakness, paresthesia, peaked T wave, flattened P wave, wide QRS

AKI labs

accumulation of waste products -> metabolic acidosis elevated BUN and Cr means intrarenal damage BUN: affected by many things, BUN-Cr ratio (20:1 indicates pre-renal cx, 10:1 indicates toxic injury) Cr: almost totally excreted by kidneys, directly r/t GFR Fractional excretion of sodium (FENa): <1% suggests pre-renal compromise >2% suggests ATN (intrarenal) K+ can be high or low, Na+ can be high or low Ca low Phos high - normally PTH helps Ca reabsorption and phosphorus excretion - renal failure = mechanisms in nonfunctional - most Ca in blood bound to protein - measured by serum Ca - Ca non bound metabolically active, measured by ionized Ca - Tx: calcium supplements, vit D supplements, lower phosphorous binders, combined with calcium salts (Phoslo), given with meal

Accessory organs

gallbladder and pancreas GB- stores and concentrates bile between meals Pancreas- produces enzymes needed for digestion of carbs, proteins, and fats; produces alkaline fluid (amylase and insulin)

Hypocalcemia (what will you see?)

muscle cramps, tetany, dysrhythmias, seizures, AKI, acute nephrocalcinosis, tingling of fingers/lips, Trousseau's and Chekhov's signs

Phases of AKI OLIGURIC

or ANURIC - <30 ml/hr or <400 ml/24h - begins within 48h of insult - lasts 5-8 day in non-oliguric - 10-16 days in oliguric - incr. BUN & Cr - incr. K, phos, decr. Ca and decr. Na!!! (dilutional) - metabolic acidosis - edema - CHF - N&V and fatigue (azotemia/urea) - incr. infection risk Tx: dialysis

Trauma

preventable disease process that is communicable "Golden hour" of trauma - access to emergent care within first hour of injury → incr chance of survival with fewer complications - Trauma must be recognized as a dz process...seasonal variations and trends, and characteristic demographic distribution...age dependent...has ID cx, est. means of tx, and defined means of prevention. - Trauma is communicable, people injure other people, attitudes toward risk-taking behavior-such as running red lights can spread in a community - Car crash instead of accident (not an accident, it is predictable and preventable dz) Trauma → SNS response (epi/NE catecholomines), baroreceptor response (incr. MAP) → fld shifts, RAAS, ADH Hypovolemic shock is most common with trauma

Jaundice

yellow/green skin caused by inc plasma bilirubin >1.2 Causes: hemolytic, obstructive, hepatocellular s/s: urine darkness, light colored stools (obstructive), yellow discoloration of sclera and then skin, pruritus Diagnosis: unconjugated bilirubinemia - hemolysis or hereditary disorder of bilirubin metabolism Conjugated bilirubin - liver injury or extra-hepatic obstruction ETOH abuse, viral exposure, gallbladder disease Treatment : underlying cause