Critical Care Exam 2

GI + Nephro SG Review for Nephro, GI and Surgery Marywood PA Program Critical Care Tuesdays at 8-10am 1. How to calculate corrections for glucose and sodium along with albumin and calcium (refer to the corrections document already on Brightspace) 2. Understand the difference between Granulomatosis with polyangiitis and Good Pastures. What s/s should the pt have? What tests should be preformed and what is the treatment? a. Granulomatosis with polyangiitis i. Triad = hemoptysis with hematuria and RBC casts. ii. Bx shows necrotizing granulomatous vasculitits. + ANCA. b. GoodPastures – autoimmune disease presents same as Wegner’s. + AntiGBM i. Treatment for Granulomatosis with polyangiitis and Goodpastures is steroids and cyclophosphamide 3. Treatment for Rhado. What prevents the formation of ferrihemate? a. Elevated CK and LA from muscle break down. b. Tx is fluid and bicarb. i. Bicarb is given if the pt has ATN (evident with elevated Crt/BUN) to prevent the formation of ferrihemate 4. Know the differences between the casts and what disease states have specific cast a. Hyaline casts are seen with PreRenal (FeNa less than 1%) b. Muddy Brown casts are seen with ATN (FeNA greater than 1%, usually greater than 2%) c. White Casts are seen with AIN (Goodpastures/ Granulomatosis with polyangiitis) 5. What is the most common location for a nephrolithiasis which could cause hydronephrosis? a. UPJ 6. What electrolyte can show long standing renal disease? a. Phosphorus 7. What are the different causes of prerenal disease, what would the serum osmolality be? What would the FeNa be? a. Decreased CO, Renal Artery Emboli, Intravascular volume depletion (ACEi/ARBs) Abd compartment syndrome b. High urine and serum osmolality c. FeNa less than 1%. Na follows water. If the pt is dry the kidney tries to retain more water. If the kidney retain more water the Na in the urine will be decreased 8. What is the most common cause of ATN? a. Most common cause of ATN is untreated PreRenal Azotemia. b. What would the FeNa be? i. If a pt has ATN the nephron is affected. Then the kidney is not able to retain water. If the kidney is not able to retain water then there will be elevated Na in the urine 9. Rhabdomyolysis is an example of what type of AKI (Prerenal/Post renal / intrinsic), What labs would you suspect to see with a pt with this disease? Why dose giving these pts HCO3 help with their renal function? a. Refer to question 3: b. Elevated CK and LA from muscle break down. Tx is fluid and bicarb. Bicarb is given if the pt has ATN (evident with elevated Crt/BUN) to prevent the formation of ferrihemate 10. Know the difference between: Hypervolemic hyponatremia vs euvolemic hyponatremia vs hypovolemic hyponatremia a. Hypervolemic Hyponatremia = excess fluid (edema). Found in cirrhosis/chf b. Euvolemic Hyponatremia = volume status normal. SIADH/Adrenal Insufficiency Addison's ds (hyper K/HypoNa/hypoglycemia) c. Hypovolemic Hyponatremia = decreased volume (dehydrated). Diarrhea and diuretics, cerebral salt wasting syndrome 11. How to hide and eliminate K? What EKG changes will you see with high K and low K? a. Hide = Insulin (D50 does nothing to K levels, just prevents hypoglycemia. If a pt already has high blood glucose, lets say they are in DKA with BS of 400) then you can give insulin without D50) i. Beta Agonist like albuterol ii. HCO3 b. Eliminate= Furosemide/Kayexalate and last measure is IHD. Remember your needs for emergent hemodialysis (AEIOU) and when you would use IHD over CRRT. i. IHD is the preferred, but if the pt is hypotensive on multiple pressers you want CRRT due to the fact that it takes less volume off at a time since its ran over 24hrs c. Emergent Hemodialysis i. Acidosis ii. Electrolytes iii. Ingestions, mediciaonts iv. Overload with fluid v. Uremia - Nausea, uremic pericarditis 12. What medications would you give during a code due to hyperK (there is one correct/best answer) ● Calcium Chloride helps stabilize the myocardium if the cardiac arrest is caused by HyperK. ● CaCl does nothing to the serum K levels it just competes with its binding to the heart muscle 13. What are Trousseau and Chvostek sign. What do these signs indicate? a. Troussau sign is when the arm contracts with a BP cuff b. Chvostek sign is when the face spasms after being tapped. i. Both signs are indications for low Ca++ levels. Remember that Ca++ levels in the serum may be falsely low with pts with low albumin 14. What are the Indications for urgent HD? a. Acidosis - metabolic b. Electrolyte – K remains elevated despite being treated (insulin hco3 lasix ect) c. Ingestion– drugs d. Overload – volume, pt not peeing e. Uremia – endocarditis or encephalitis 15. IHD vs CRRT, what are the benefits and drawback for each a. IHD treatment only last 6hrs i. less exposure to heparin/anticoagulation products ii. more likely to cause hypotension due to massive volume shifts b. CRRT – lasts 24hrs used for pts on pressers. i. Longer exposure to heparin/anticoagulation so the blood doesn’t clot in the machine 16. What is a nonlab value way to assess the Mg++ levels in a pt? a. DTR. Mg levels have an inverse relationship with reflexs 17. What are the indications for Foleys? a. Close monitoring of I/O in hemodynamically unstable pt b. Desaturation of ventilated patient if moved c. Decubital Ulcers >3 d. Palliative Care/Comfort Measures e. Urethral damage from frequent straight caths 18. What is the most common cause of fulminate hepatic failure, what is the treatment for the most common cause? a. Tylenol toxicity is treated with NAC if ingestion happens after 4-6hrs after ingestion. If ingestion is within 4-6hrs then give activated charcoal 19. How do you treat elevated levels of ammonia? a. Lactulose 20. What could cause elevated BUN levels on a basic metabolic panel besides intravascular depletion/prerenal azotemia, and why? a. GI bleed 21. Hepatitis B antigen/antibodies- who has an active infx, who is immune, who has been cured? Anti HBc = core antibody Anti HBs = surface antibody HBsAg = surface antigen a. If HBsAg (antigen) is present – infection is present i. If no antibody is present – acute infection ii. If IgM is present – early infection iii. If IgG is present – chronic infection b. If just Anti-HBs antibodies present – vaccinated against disease (makes sense because HBs is in the vaccine) c. If Anti-HBs AND Anti-HBc – cleared infection (makes sense because both of these are present in the virus responsible for the acute infection) d. If all negative – not infected/not immune 22. What type of fluid resuscitation should you give for a pt who became hypotensive after a paracentesis and why? a. 25% albumin is the best tx for hypotension after a paracentesis due to the fact that it has oncotic osmotic gradients. That will cause not only volume to stay in the intravascular space longer (when comparted to isotonic solutions) but will also bring some of that 3rd spaced fluid back into the intravascular space. 23. Upper GI bleed: What is the most common cause? What is the treatment for the most common cause? What should be given if the pt has a hx of portal htn/cirrhosis? If the pt continues to bleed despite the addition of these 2 medications what other intervention can be given and what is a complication if that device is left in for too long or if it is over inflated? a. Most common cause of UGI bleed is PUD – all pts with UGI bleed should be treated with PPI like protonix. b. If a pt has signs of cirrhosis (portal htn/caput medusa/ scar tissue on CT) and they have an UGI bleed they should be treated with PPI and Octreotide. Octreotide will help decreased pressure within the portal veins. c. If bleeding continues and the pt has cirrhosis you can place a Blakemore/Minnesota tube. These tubes are placed into the esophagus and stomach then a balloon is inflated. Once the balloon is inflated it will cause tamponade affect to the bleeding vessels. This is only a temporizing measure until an EGD can be preformed due to the risk of esophageal necrosis 24. Hematemesis vs coffee ground vs melena vs hematochezia vs BRBPR. Understand the differences and what disease they are associated with a. Hematemesis = vomiting of blood usually indicates an UGI bleed – above the ligament of Treitz b. Coffee ground = Digested blood- UGIT c. Melena = passage of black tarry stools due to the digestion of blood by acid and bacteria. Usually from the UGIT but may be 2/2 bleed in the Right Colon d. Hematochezia = fresh blood per anus - 90% comes from the lower GIT but found in some cases of massive UGI bleed e. Hematochezia – when blood mixes with fecal matter. Stool turns dark and smears very easily. Can be confused if pt took bismuth. +FOBT f. BRBPR = distal GIT/Hemorrhoids i. ABCD are associated with upper GI bleeds while E and F are associated with lower GI bleeds. ii. Remember the anatomical location that separates upper from lower GI bleeds is the Ligament of Trietz 25. What anatomic location is used to differentiate between upper and lower GI bleeds? a. See question 24 b. Hematemesis = vomiting of blood usually indicates an UGI bleed – above the ligament of Treitz c. Coffee ground = Digested blood- UGIT d. Melena = passage of black tarry stools due to the digestion of blood by acid and bacteria. Usually from the UGIT but may be 2/2 bleed in the Right Colon e. Hematochezia = fresh blood per anus - 90% comes from the lower GIT but found in some cases of massive UGI bleed f. Hematochezia – when blood mixes with fecal matter. Stool turns dark and smears very easily. Can be confused if pt took bismuth. +FOBT g. BRBPR = distal GIT/Hemorrhoids i. ABCD are associated with upper GI bleeds while E and F are associated with lower GI bleeds. ii. Remember the anatomical location that separates upper from lower GI bleeds is the Ligament of Trietz 26. What abx and bacteria is associated with recurrent PUD? a. H pylori is dx with Urea breath test and bx of the ulcer. Treatment is Metronidazole 27. MELD vs Child-Pugh score are used to calculate the mortality of what disease state? a. Liver. b. MELD is used for need for TIPS procedure ( used to prevent recurrent UGI bleed from eso varices) i. Remember if a pt has a TIPS procedure it may help prevent UGI bleeds from eso varices but it can cause elevated Ammonia levels causing AMS c. Child- Pughis used for need for liver transplant 28. Understand the differences between UC vs Crohns a. Slides 37 on GI lecture 29. Understand the differences between TF vs TPN and what types of patients would benefit from this type of nutrition a. Slide 53 on GI lecture 30. Besides elevated abdominal pressures (>20mmHg), what must a pt have in order to be dx with abdominal compartment syndrome? a. Renal disease- evident with elevated Crt/BUN and or decreased UOP (less than 0.5ml/kg/hr) 31. What are the most common causes of acute pancreatitis? a. Most common cause of pancreatitis is EtOH abuse and gallstones 32. What disease is associated with Charcot’s triad and Reynolds pentad, and what are in each a. Charcot’s Triad = Right Upper Quadrant pain/ Jaundice/ Fever b. Reynold’s Pentad = Charcot’s Triad + hypotension and confusion c. Seen with Acute Cholangitis 33. What are the risk factors for refeeding syndrome? If you were to feed these pts with a high caloric diet, what labs would you expect to see? How do you precent refeeding syndrome? a. RF = Anorexic/Elderly/EtOH abuse b. If these pts are given high caloric intake their lytes will shift inside the cell resulting in low: Ca/Phos/K/Albumin which can result in cardiac arrest. c. In order to prevent refeeding syndrome caloric intake should be started at 50% the calculated daily needs and slowing increased while following serial chemistries and aggressive replacement 34. What can be given to pts with hypertriglyceridemia to increase the synthesis of hydrolysis of triglycerides? Why should these pts be given anticoagulation? a. Insulin promotes hydrolysis of Fatty Acids. This should be given in the acute setting. It will decrease triglycerides fast. b. Pts should be started on systemic anticoagulation to prevent embolic events. With extremely high triglyceride levels there is “fat balls” that are in the vessels which can cause strokes/pe. 35. What beta blocker should be given to pts with recurrent upper GI bleeds that are hemodynamically stable? a. Propranolol should only be started with pts with recurrent upper gi bleeds if they are hemodynamically stable. It is a Beta blocker which can worsen bp 36. Know the different types of TBI SAH,SDH,EDH. If a vein or artery is affected and what they look like on CT head a. SDH – crescent shape, bleeding veins, AMS gradually increase, Bleed crosses sutural margins. Looks like banana i. Bridging veins b. EDH- arterial bleed, doesn’t cross sutural margins, pts are altered then have lucid interval of clarity then AMS again i. Arteril 37. How do you decrease ICP a. Hypertonic Na- takes longer time to get to goal Na 150 (when compared to mannitol), isn’t affected by volume status. b. Mannitol – Rapid onset but should avoid with pts who are hypotensive, hypovol c. Hyperventilation – Low CO2 levels causes cerebral vasocontraction which can result in cerebral ischemia after prolonged periods of time and should only be used for the first 6 hrs. Goal less than 25 PaCO2. d. Position = Pts should have the HOB at least 30 degrees. Which improves venous returns. Review Cases Interpretation for Hepatitis B Anti HBc = core antibody Anti HBs = surface antibody HBsAg = surface antigen Case 1 A 39 year old female presents with altered mental status and abdominal pain. Labs are grossly unremarkable except for an elevated ammonia and elevated LFTs. A review of her PMH reveals she has been an alcoholic and is a former IV drug user. You review her immunization history which only shows that she has gotten the flu shot. Glucose 140. Drug screen negative. Head CT shows no acute process. You order a hepatitis panel which shows: ⇒ Anti HBc-IgM negative, Anti HBs-IgG positive, HBs positive, Anti HBS negative Interpretation of Hep B Results ? ● Chronic hepatitis B Why would this patient be confused? ● Ammonia What is the Treatment? ● Lactulose ○ Lactulose should be avoided in patients who do not have normal BM - potential rupture ○ 3 Bowel movements/Day ○ Only 2 BM? ⇒ Increase the dose ● Antibiotics ⇒ Rifaxamin ○ Decreases gut bacteria to decrease ammonia that is produced ● If ammonia is above 200-500 ⇒ May require dialysis Case 2 A 46 year old male presents to the ED with the chief complaint of hematemesis. It is noted that the patient has a significant history of alcohol use (about 20 beers daily since his wife left him 2 years ago). He has no other PMH of noted other than a recent DVT for which he was put on coumadin. He is not on any other medication. The patient has been following up with his primary care doctor who recently ran a hepatic function panel which was unremarkable. Previous Hgb was 14.0. Repeat labs in the ED shows a Hgb of 6 and INR 2.8. Lactic acid 4.0 Physical examination shows the patient is tachycardic and tachypneic and hypotensive with a BP of 80/40. Abdominal exam shows engorged veins surrounding the umbilicus. What do you think is the potential causes of this bleed? ● Upper GI bleed What anatomical marking separates upper from lower GI bleeds? ● Ligament of Treitz What is the most common cause of upper GI bleeds? ● Peptic Ulcer Disease What medications would you want to start with this pt? ● Octreotide - Portal HTN ● All patients should be started on a PPI - Protonix How do you reverse coumadin? ● Vitamin K ⇒ 2,7,9,10 What if the pt has an EGD that is negative for any bleeds what other test can be preformed to role out lower GI bleeds? ● Tagged RBC Scan/Nuclear scan: Used to find etiology of LGI bleed ○ If positive, send to IR ⇒ Cauterization NOTES: Treating Portal HTN: ● If patient is hemodynamically stable ⇒ Start patient on Propranolol If patient has recurrent esophageal variceal bleeds ⇒ Consider the TIPS procedure ● TIPS = Transjugular Intrahepatic Portosystemic Shunt ● Used to reduce GI bleeds in patients with Cirrhosis ● MELD Score (Model of End-Stage Liver Disease): Predicts the mortality in the first 3 months after a TIPS procedure and is now used to predict the necessity of liver transplant ● This is only a temporary measure. By bypassing the portal system it can cause elevations in ammonia causing AMS Case 3 56 yo male who presented to the ED with R upper ext weakness with slurred speech that started approx. 2 hrs prior to arrival. Pt stated that he was just setting down eating dinner and this weakness started suddenly. He denies any trauma prior to onset of symptoms. In the ED, the pt is evaluated if he has is AAOx3 following commands, tolerating RA with a SpO2 of 98%, RR10 unlabored, Hr 95, bp:126/84, and has a NIH score of 15. A “Stroke Alert” is called and the pt is taken emergently to the CT suite to get a non-contrast imaging of the head and CCM is consulted. What will you see on a CT of acute ischemic stroke? ● Nothing ● If it is black or shows necrotic tissue, it is too late for TPA Where is the likely location of the ischemic CVA? ● ACA = contralateral leg w. behavior changes ● MCA = contralateral face and arm, dysarthria, visual changes, sensory defects (MC) ● PCA = visual deficit and sensory deficits ● Vertebrobasilar = dizziness, ataxia, change in voice and swallowing What NIH score should be given tPA? ● 0-4 No tPA ● 4-20 give tPA ● >20 No tPA Does this pt meet the criteria for tPA? ● Yes, NIH is good and approbation onset ● Onset of S/S within 3-4.5 hours ○ (Last known well) What should be included in the stroke work up? ● Echo to r/o structural abn (VSD) ● EKG r/o Afib ⇒ MCC is Afib - CHADS2 VASC ● Carotid duplex ⇒ Check for stenosis ○ Carotid Duplex = Stenosis >75% ● Lipids Case 4 You are called to the psych floor for an RRT. The pt is a 35 yo female who was admitted 3 days prior for severe depression. The RRT was called for hyperactive delirium with severe muscle spasms/rigidity. You evaluate the pt to find that she is awake and agitated but not following commands. Physical exam shows that the pt is tachycardic with a bp of 140/89. She is tolerating NC with acceptable SpO2 and RR but her muscles are incredibly “stiff”. You decide to transfer the pt down to the ICU for close monitoring. While the pt is getting transferred down to the unit you perform a “chart check” and see that the pt is on citalopram, fluoxetine, and escitalopram. What do you think is the cause for this pts presentation? ● Serotonin Syndrome What labs/images do you want to perform? ● Head CT ● CK (also CBC and BMP) ● LA ● EKG to r/o prolonged Qtc ○ If QTC > 500, do NOT give psych meds, If they have a pulse give magnesium What medications do you want to start? ● NSS ● Lorazepam/Ativan for agitation ● Cyproheptadine ⇒ Reverses Serotonin Syndrome ○ a serotonin an antagonist If the pt develops a fever that doesn’t respond to acetaminophen/ibuprofen and cooling blankets what medication should be started? ● Dantrolene NOTES: ● NMS and SS usually present the same way ○ Hyperactive delirium with muscle rigidity ○ But SS usually have an abrupt onset of s/s. +elevated DTRs ● The best way to dx SS is to do a chart check and see what medications the patient is on. ○ SSRIs, TCA, Lithium, Amphetamines, MAOIs all can cause SS ○ Treatment should include cyproheptadine. ● Both NMS and SS treatment include remove offending agents and give fluids. ○ Ativan/lorazepam can be given for agitation ○ Recalcitrant fevers should be treated with dantrolene. Critical Illness Myopathy (CIM) - (from not using muscles) ● ● ● ● ● Diffuse inflammatory myopathy that involves both limb and truncal muscles, causing diffuse flaccid weakness in the limbs and even the diaphragm. Predisposing conditions: Severe sepsis, septic shock, and prolonged periods of drug induced neuromuscular paralysis, particularly when combined with high doses of steroid therapy. Treatment = None, supportive. Complete recovery is expected but can take months. May need prolonged vent support Paralytics ○ Nondepolarizing agents: Rocuronium/ Vecuronium/ Nimbex ■ No K+ shift ○ Depolarizing agents: Succinylcholine (caution with Renal Failure/Burn/Crush Injuries) ■ Causes fast shifts of K+ upside of cell ⇒ Likely to cause arrhythmias Prevention ○ Decrease steroids ○ Physical Therapy Case 5 Pt is a 34 yo female with a pmhx significant for trisomy 21, epilepsy, CKD and hypothyroidism. She came to the ED unresponsiveness with her mother who stated that pt has not been taking her AED medications like she should due to insurance issues. GCS is noted to be 6. She was subsequently intubated for inability to protect her airway. Head CT is negative for any acute pathology. The ED started the pt on a midazolam/versed infusion. As the lab work is “cooking”, CCM is consulted. You go down to the ED with your attending, who immediately stops the midazolam infusion and changes sedation to propofol. What is the probable cause for this patients AMS? Why did your attending change sedation from versed over to propofol? ● Propylene Glycol toxicity = hyperosmolarity & anion gap metabolic acidosis, often accompanied by AKI which can eventually progress to MODS (multiple organ dysfunction syndrome) ○ Propylene Glycol is used the convent for IV Lorazepam and Diazepam What should you watch out for with the infusion of propofol? ● PRIS = Characterized by Rhabdomyolysis/ Bradycardia with Junctional Rhythm/ Anion Gap Acidosis What labs should be obtained? ● CBC/BMP/ LA/ CK What is the normal treatment for a patient in status? ● Lorazepam/Midazolam first line ● Followed by fosphenytoin ○ Valproic acid if allergy to phenytoin What should your goal RASS be for this patient? ● (-1) to (-2) Case 6 18 yo male presents to the ED with a cc of lower ext weakness that is slowly progressing up the pt’s legs. A pmhx shows that the pt received the flu shot 2 wks prior. What disease is the likely cause of the ascending weakness given this pt’s pmhx? ● Guillain Barre What medication should be given? ● Plasmapheresis/IVIG NOTES: Bilirubin ● In the reticuloendothelial system, hemoglobin is broken down into heme and globin. Heme is further broken down by 2 enzymes hemeoxygenase and biliverdin reductase. Forming bilirubin and Fe+. Fe+ and globin are recycled to form new hemoglobin through erythropoiesis. ● Bilirubin currently is unconjugated (indirect) bilirubin that is lipid soluble. It binds to albumin and travels to the liver. ● With the unconjugated (indirect) bili in the liver it goes into glucuronidation via the uridine glucuronyl transferase enzyme (UGT). Glucuronidation makes the bili water soluble, so it can be eliminated bile and urine. ● Conjugated (direct) Bili in the GIT gets converted with urobilinogen which gives the stool its brown color and urine its yellow color. Elevations of Bilirubin ● ● ● ● Unconjugated (indirect) elevations: extravascular hemolytic anemias(DIC/Rhabdo) or ineffective hemopoiesis = sickle cell. Neonatal Jaundice = phototherapy. Gilberts syndrome/ Crigler Najjar Syndrome. Conjugated (Direct) elevations: obstructive jaundice – gall stones pancreatic cholangiocarcinoma, liver fluke. Can cause pruritis, cholesterolemia, xanthomas ○ Can cause decreased absorption of fat and steatorrhea (oily stools) Gilberts disease = decrease glucuronidation enzyme (UGT). Crigler Najjar Syndrome = No UGT, usually fatal causing kernicterus Myasthenia Gravis vs Guillain-Barre Synrome Treatment for Myasthenia Gravis ⇒ Pyridostigmine Case 7 34 yo male presents to the ED after a suicide attempt. He stated that he went into his parent’s medicine cabinet and took an unknown amount and type of pills. In the ED he is found to have a Hr 120, Bp 150/80. He is tolerating NC with acceptable SpO2 but has a RR 30, temp is noted to be 101.2. The pt is agitated stating that he is having blurry vision. Head CT is preformed which negative for any acute pathology. Drug Screen returned back negative for opioids/ cocaine/ methamphetamines/ benzos and marijuana. CCM is consulted at this time due to unclear dx. Given this pt’s presentation what is the likely dx for an overdose? ● Anticholinergics If the pt was + for Opiods what would you give? ● Naloxone Bolus vs GTT What should be given if the pt admitted to overdosing on and + for benzos? ● Flumazenil What should be given if the pt admitted to overdosing on metoprolol? ● Tx: Atropine, Glucagon ● Cardiac pacing, ECMO What should be given if the pt admitted to overdosing on Cardizem? (calcium channel blocker) ● Calcium Chloride NOTES: ● All overdoses should be considered polysubstance until proven otherwise. ○ EtOH and Opioids should be considered part of the polysubstance Substance S/S Diangoses Treamtent Opioids Sedation/hypercarbic resp failure Mostly clinical. Urine drug tox Naloxone bolus vs gtt Acetaminophen Asymptomatic, N/V, Liver Failure Serum Acetaminophen levels Activated Charcoal if ingestion is less than 4hrs PTA Salicylates Abd pain, N/V, Metabolic Acidosis (MUDPILES) Salicylate Level Alkalization of the urine, HD Tricyclic Antidepressants Anticholinergic toxidrome -Mad as a Hatter/Red as Beet/ Blind as a Bat/Dry as a Bone/ Hot as a Desert Prolonged Qtc and TCA use hx IV sodium bicarbonate/ Physostigmine Bet Blockers Bradycardia/ hypotension Clinical Dx Atropine, Glucagon, cardiac pacing, ECMO Calcium Channel Blocker Bradycardia/ hypotension Clinical Dx Calcium Chloride Cocaine Hypertension/ Tachycardia Clinical hx, urine drug screen Benzos/Anti HTN (except for BB) – Nitroglycerin/Nitropru sside Cocaine causes excitement of both the alpha and beta receptors; BB will only block the Beta receptors. Nitroprusside (especially in renal failure) S/S of cyanide toxicity: Tachycardia/confusio n/tachypnea Treatment: Hydroxocobalamin and sodium thiosulfate Benzodiazepine S/S: Sedation/hypercapnic resp failure Dx: Pmhx ?Suicide Note Tx: Flumazenil Case 8 23 yo male presents to the ED due to abdominal pain. He has a pmhx sig for uncontrolled DM (last A1C = 12) and noncompliance. In the ED he gets lab work that shows CT Abd and pelvis are preformed which are negative for any acute pathology Why is the pt having abd pain? ● Gastroporesis Interpret the ABG? Why is the pt acidotic? ● Patient is Acidotic due to the ketones What is the corrected Na? (always check sodium when glucose is elevated!) 2.4 (serum glucose -100)/100 2.4 x (900-100)/100 2.4 x 8= 19.2 19.2 + serum Na (130) = 149 What fluid should be used for this pt given the corrected Na? ● ½ Normal Saline (corrected Na is high) What treatment should be started with this pt. (order is important!)? 1. Fluids - Correct Na 2. Fix Potassium - 10 Meq (insure K is correct before starting insulin 3. Slowly correct glucose with Insulin - 50-100/ hour a. Too much can cause Cerebral edema (treat with mannitol) NOTES ● DKA usually occurs in pts with Type 1 DM ● HHNK usually occurs with pts who have Type 2 DM. ● Add D5 @ 250, continue insulin ● Take off insulin when there is no anion gap acidosis ● Transition to long acting insulin Case 9 26 yo male was brought into the ED with a cc of AMS. The pt was found down surrounded with needles. He doesn’t have any significant pmhx except for IVDA. Vitals: 105/60, rr 6 unlabored, Hr 60. SpO2 94% on NRB GCS 3. He was given Narcan but no response was noted. ED decided to intubate him. For RSI he was given rocuromun, no other medications were given. After intubation the pt is oxygenating well. Post procedure CXR shows acceptable placement of ETT without any gross cardiopulmonary pathology. CCM is consulted. When you arrive you notice the pt is now tachycardic with a hr 160 and hypertensive 180/110. EKG confirms ST What is the treatment for this pt with ST and hypertension would you give the pt? ● Do NOT give labetalol/metoprolol ⇒ TREAT PATIENT NOT NUMBERS ● Give them sedative ○ Fix the sedation and the tachycardia and hypertension will resolve Why is the pt hypertensive and tachycardic? ● Because the patient is not adequately sedated Case 10 Pt is a 32 yo female who presents to the ED with AMS. She is a cachectic female who appears to be severely malnourished with bitemporal wasting. She has a hx of EtOH and IV abuse. She was intubated for failure to protect her airway; despite being given Narcan. Head CT is negative for any acute pathology. She is transferred up to the ICU for further care. Drug screen returned back + for methamphetamines and ammonia levels were noted to be elevated. While in the unit, she is connected to an EEG to r/o nonconvulsive status. Lab work at the time of admission shows K3.5/ Na 135/ Ca 7.8 with a glucose of 45 and a phos of 3.2. While in the unit she is started on fent prn bolus for vent compliance. TF are also started. What should be replaced? ● Potassium ● Glucose (140-180) The following day repeat labs show K 2.5/ Ca 6.2/ Na 120/ Glucose 140 and Phos 1.4 Why are the lytes abn worsening? ● Refeeding syndrome ● 150 of potassium NOTES: ● Labs: ○ ○ ○ ○ ● Patho ○ ● Hypocalcemia Hypophosphatemia Hypokalemia Hypoalbuminemia When carbs are given to malnourished patients, lyle’s can shift into the cell (PO4, K, Ca) ⇒ Diaphragmatic problems ⇒ Respiratory problems Treatment ○ Controlled increase of caloric intake ○ Starting at ½ of caloric needs and increasing steadily over a period of days ○ Replacement of Lyte abn. Case 11 Pt is a 56 yo male with a pmhx significant for Afib on Coumadin and HTN on labetalol. The pt is brought into the ED with a cc of general malaise s/p fall. Vitals Hr 110, BP 90/45, RR 12. Temp 96F. PE: lungs are CTA/ Heart sounds are irreg irreg. abd + BS nontender. + ecchymotic mass on L LE. Pt is found to be lethargic, only opening eyes to pain, nonverbal and extension of extremity to pain. POCUS is preformed which shows a hyperdynamic LV Lab work: Hgb 5.4, INR 3.5, plt 400 AST 20/ ALT 30, BS 120 Drug Tox negative. What is the first thing you want to do? ● Maintain Airway ● GCS < 8 What type of Shock is this? ● Hypovolemic Shock What further images are needed? ● Head CT **Reverse Coumadin with vitamin K The pt is intubated for poor GCS. After the airway is secured you give Vit K along with 2uPRBC. After blood is given the pts BP 110/56 with a MAP of 74. You start the pt on propofol for ventilator compliance. Head CT is obtained which is unremarkable. Post intubation ABG pH 7.40/Co2 35/ PaO2 150 on a PEEP of 5 and FiO2 of 50%.The pt is admitted into the unit for further care. While in the unit, the RN calls you to the room for acute onset of hypotension and hypoxia. BP currently 84/45 with a SpO2 85%. The patient remains on the same vent settings PEEP 5/FiO2 50%. Auscultation of lungs is concerning for b/l rhonchi. Repeat Lab work is obtained Hgb 7.5,INR 1.2. ABG pH 7.39/CO2 39/ PaO2 80 What's on the DDx? ● TRALI - Transfusion Related Acute Lung Injury ○ New acute lung injury/ARDS occurring during or within six hours of blood product administration ○ Presents with: hypoxemia (change in O2 requirement in intubated patient), pulmonary infiltrates on CXR, pink frothy airway secretions from ETT, fever, hypotension ○ Treatment: Discontinue transfusion, alert blood bank, O2 supp., increase BP ○ Change propofol to fentanyl ● TALI has HYPOTENSION ● TACO has HYPERTENSION Case 12 Tom is a 67 yo male who was admitted into the ICU after a scheduled cardiac cath where they placed a stent after a routine EKG showed elevations in the inferior leads. In the ICU the patient is started on systemic heparin for his hx of Afib, previously on Eliquis, along with Plavix and ASA. The pt is awake alert following commands moving all ext. Temp is 36F RR 10, BP 110/85, Hr 67 (irreg irreg) Lab work showed: On day 3 of being in the ICU, you examine the patient and see that he has a petechial rash. Morning lab work showed: What is on the DDX? ● HIT - Heparin Induced Thrombocytopenia ● TTP ● AKI What other labs should we get to help confirm the dx? ● HIT ELISA immunoassay (anti-PF4 antibodies) ● SRA - Serotonin Release Assay (definitive) ● ADAMAS13 NOTES: ● Results from IgG binding to platelet factor 4 which causes activation of the platelets. With widespread activation of platelets there is thrombocytopenia and the formation of a prothrombotic state. ● Occurs 5-10 days after initiation of heparin ● Treat prior to tests coming back if high suspicion ● Treat with different anticoagulation (Argatroban) Case 13 You admit a 25 yo female with a weight of 50kg. The pt presented to the ED with a cc of dysuria. UA is + for esterase. She is hypotensive but responds to the initial fluid resuscitation. She is started on Bactrim and admitted into the floor for further care. While on the floor an RRT is called. You examine the patient. Hr 120 sinus tach, RR 12, SBP 75/35. Temp 101.2. You see that the patient has widespread blistering of the anterior and posterior of the chest abd and face. What is the cause of hypotension? ● Hypovolemia vs Distributive Shock What do you want to do? ● Fluids ● Isolate ● Lactated ringers 2nd degree burns to anterior chest and abd (18%) and posterior chest and abd (18%) including face (9%). Weight 50kg 4mL x (body surface burned x weight) ⇒ 4mL x (18%+18%+9%)x 50kg = 9L 4.5L in first 8hrs or 562mL/Hr x 8hrs 4.5L over the next 16hrs or 281mL/Hr x 16hr NOTES: SJS/Burn Treatment ● Concern of compartment syndrome ○ 6 Ps: Pain out of proportion, parenthesis, paralysis, pulsnessess, pallor, poikilothermia ○ Labs: Elevated CK and Lactic Acid ○ Treatment: Aggressive guilds, prophylactic antibiotics, topical ointments with silver ● First Degree – erythematous base with no bullae formation. Burn only to the epidermal layer usually found with sunburn. ● Second Degree (Partial thickness)- + bullae formation. Burn extends to the dermal layer. May need skin grafting depending on % ● Third Degree (Full thickness)– burn extends to the muscle layer + eshar. Burned area is usually painless due to damage to the nerves. Requires debridement of burned area along with muscle flaps Other Material from the Review WHAT ARE THE INDICATIONS FOR EMERGENT HD? ● A – Acidosis ○ Metabolic ⇒ Consult Neurology! ● E – Electrolytes ● I – Ingestions, medications that can be dialyzed out ● O – Overload with fluid ● U – Uremia – this usually refers to uremic pericarditis ○ One of the most common uremic symptoms is nausea. ○ Uremia can also lead to encephalopathy Difference between IHD vs CRRT. ● HD is the “normal” type of HD that happens over 4-6 hrs. This relatively short time causes massive fluid shifts and can result in hypotension ● CRRT happens over 24 hrs, requires a specialized nurse, more likely to result in bleeding due to the need for more anticoagulation, is reserved for patients who are already hemodynamically unstable on multiple pressers due to smaller amount of fluid shifts. PreRenal/Intrinsic/PostRenal Azotemia Azotemia Cause Prerenal Azotemia ● **MCC of AKI** ● ● Due to reduced renal perfusion without cellular injury Decreased GFR/Elevated Crt and BUN are physiologic responses to decreased perfusion of the kidney. If perfusion is restored, then renal funct has the potential of returning to “normal”. Etiologies ● ● ● ● Post-Ren al AKI ● ● Intrinsic Azotemia ● ● ● Caused by obstruction (intrarenal or extrarenal) of urinary flow that causes “build up” of urine within the ureters/bladder Which in turn causes a decreased GFR. ● ● Injury is found within the kidney parenchyma itself. Two different types of Intrinsic Azotemia: Acute Tubular Necrosis (ATN) ● ● *Decreased CO/Emboli Renal Artery *Intravascular volume depletion (albumin vs nss/sepsis/trauma) *Impaired Renal Autoregulation (ACEi/ARBs) *Abd Compartment Syndrome (Intra-abdominal pressure >20mmHg) Labs ● ● Rapid infusion of isotonic fluids/ avoid nephrotoxic medications/ reversing cause of prerenal AKI. Obstruction can be unilateral or bilateral. Unilateral obstruction doesn’t lead to renal failure. Anuria is only found in bilateral obstruction. ● CT Abd/Pelvis = Nephrolithiasis Post Void Residuals/Obstru cted Foley Most common cause of intrinsic azotemia is untreated prerenal azotemia, resulting in ATN. ● ● ● +/- Hyaline casts. Urine and serum Osmolality is high FENa less than 1% Treatment ● Muddy brown casts = ATN (90%) White casts = AIN ● Acute Interstitial Nephrosis (AIN) Different Casts Muddy Brown Casts ATN (90%) Red Blood Cell Casts Glomeruli White Casts AIN FENa ● Helps to evaluate the cause of acute kidney failure: ○ Below 1% is prerenal disease ○ Above 2% acute tubular necrosis or other kidney damage Indications for Foleys ● Close monitoring of I/O in hemodynamically unstable pt ● Desaturation of ventilated patient if moved ● Decubital Ulcers >3 ● Palliative Care/Comfort Measures ● Urethral damage from frequent straight caths Rhabdomyolysis ● Hereditary = deficiency in Carnitine – an enzyme that converts ATP from fatty acid oxidation ● Nonhereditary = Trauma with large amount of tissue damage/sepsis/medications (statins/cocaine), or anaerobic glycolysis during exercise ● ● Signs and Symptoms ○ Nausea ○ General Malaise ○ Dehydration ● Labs ○ Elevated CK ○ Hyperkalemia ○ Hyperphosphatemia ● UA ○ +Blood but no erythrocytes ● Treatment ○ IV hydration!! – improves solubility of byproducts of muscle degradation and improves UOP. ○ Alkalization of urine – improves solubility of myoglobin which decreases damage to the renal tubules. ■ IF renal complications occur ■ Prevents Ferrihemate formation ■ Myoglobin itself is not toxic to the nephron. Myoglobin becomes toxic when it gets converted to ferrihemate due to the acidic environment of the urine Different Types of Hyponatremia ● Hypervolemic Hyponatremia = excess fluid (edema). Found in cirrhosis/chf ● ***Euvolemic Hyponatremia = volume status normal. SIADH/Adrenal Insufficiency. Addisons ds ● (hyper K/HypoNa/hypoglycemia) ● Hypovolemic Hyponatremia = decreased volume (dehydrated). Diarrhea and diuretics, cerebral salt wasting syndrome ● PseudoHyponatremia – falsely low Na on the labs usually due to hyperglycemia found commonly with DKA < HHNK. Can be due to triglycerides/proteins’ HyperKalemia ● Most common cause of hyperK is decreased renal filtration, then iatrogenic, crush injuries ● EKG= peaked T waves/ decreased amplitude or complete loss of the P waves prolonged/increased PR interval/ prolongation of the QRS/ AV conduction delays. ● Treatment: Hiding vs Eliminating ○ CaCl – stabilizes myocardium (doesn’t affect the concentration of K in the serum) ○ Insulin – causes extracellular K to move intracellularly. Ensure you give D50 prior to insulin to prevent hypoglycemia ○ Beta Agonist – Continuous inhale albuterol treatment. Indirectly activates Sodium Potassium ATPase on the cellular membrane causing K to enter the cell ○ HCO3 – causes intracellular shift of potassium ○ Lasix – helps with the Elimination of K via the kidneys. ○ Kayexalate – causes K to be Eliminated through the GI tract. Kayexalate can cause gut perforation. Contraindicated for SBO ○ HD elimination of K and other metabolites/electrolytes via a synthetic kidney ○ Treat SLOWLY (4-6 Meq/24 hours) ■ Prevent swelling in the brain ○ What is the best mediation to HIDE K? UTI ● ● Bacteria is needed for a positive Test ○ Clean Catch: Low to No Epithelial tissue present in sample means it is NOT contaminated. Bacteria needs to be >100,000 cfu/mL ○ Foley: Bacteria >100 cfu/mL ○ Suprapubic = if any bacteria is present then its + Labs ○ Elevated white count UA= +Ketones/Bacteria/Pus/ Bacteria degree (to consider to have bacteriuria) is dependent on source of Urine ○ Gram Negative Bacteria (E coli) is the most common pathogen. Ulcerative Collitis vs. Chron’s Organs Affected By Retroperitonieal Bleed (SAD PUCKER) ● Suprarenal glands (adrenals) ● Aorta ● Duodenum ● Pancreas ● Ureters ● Colon ● Kidneys ● Esophagus ● Rectum ● Which is not in retroperitoneal acuity? Types of GI Bleeds ● Hematochezia – when blood mixes with fecal matter. Stool turns dark and smears very easily. Can be confused if pt took bismuth. +FOBT ● BRBPR = distal GIT/Hemorrhoids ● Hematemesis = vomiting of blood usually indicates an UGI bleed – above the ligament of Treitz ● Coffee Ground = Digested blood- UGIT ● Melena = passage of black tarry stools due to the digestion of blood by acid and bacteria. Usually from the UGIT but may be 2/2 bleed in the Right Colon ● Hematochezia = fresh blood per anus - 90% comes from the lower GIT but found in some cases of massive UGI bleed - Since PUD is the most common cause of UGIB all pts with suspected UGIB should be started on PPI. If a patient has recurrent PUD ⇒ You should be concerned about H pylori infection - H Pylori Testing: Urea Breath test/Bx - Treatment: metronidazole (Flagyl)/clarithromycin ADVANTAGES AND DISADVANTAGES WITH FEEDINGS TABLE Acute Choangitis ● Morbid condition that is characterized by acute inflammation and infection in the bile duct. Usually associated with obst of the biliary tree, which could result in sepsis and multisystem organ failure. ● Common causes of infection result from bacteria from the duodenum entering through the sphincter of Oddi which can result in the seeding of bacteria in the biliary tract and into the portal system. ● Common bacteria E. coli (25-50%)/ Klebsiella (15-20%)/Enterobacter (5-10%) ● Abx = fluoroquinolones (levofloxacin) and metronidazole/ Flagyl ● Charcot’s Triad ○ Right Upper Quadrant pain ○ Jaundice ○ Fever ● Reynold’s Pentad ○ Charcot’s Triad ○ + Hypotension and confusion ○ Imaging ■ US Abd = best initial imaging study for it can see dilation and the presence of stones ■ CT Abd = can see dilation of the bile ducts but more difficult to see obstruction ■ ERCP Can both visualize the bile duct and remove any potential stones and insert stents. Hypertriglyceridemia ● Do not have specific s/s. May have eruptive xanthomas. ● Most often dx via lab work. ○ +1000 triglycerides ● Check Pancreatic Enzymes, Lipase (hydrolysis of TG) and TSH/T4 (metabolism) ● Treatment: ○ Stop medications/foods that could increase triglycerides ○ Start statin therapy. Monitor CK ○ Start IV insulin therapy add D5 gtt if hypoglycemic ■ insulin promotes the synthesis of lipoprotein lipase which also helps with the hydrolysis of TG into fatty acids and facilitates the storage of the fatty acids into adipocytes ■ Watch glucose!!!! ● ○ Start heparin gtt therapy ○ Consider plasmapheresis (if all else dIls) NICE Study ⇒ 140-180 is the ideal glucose in the ICU Brain Deaht Criteria ● Brain Death = irreversible coma, with a known etiology, accompanied by loss of all brainstem reflexes and absent respiratory drive. ● Etiology= ICH/hypoxia 2/2 cardiopulmonary arrest/cerebral trauma/meningitis/ cerebral edema that causes ischemia. ● Should be done by 2 different professionals 12hrs apart, unless expert. Testing For Brain Death (know the part of the brain that correlates to PE) ● Deep Painful stimuli – No withdrawal/No posturing/No seizure activity ● Pupils are not reactive to light - Midbrain ● Caloric Test – Vestibular (COWS for intact brainstem) (drops in the ear) ● No corneal reflex - Pontine ● No gag reflex – Medulla ● Apnea Test – Obtain ABG before and after. Changes in pCO2. (pO2 changes doesn’t matter, problem with ventilation not oxygenation) ● DTR preserved. Lazarus Sign – Abdominal flexion/abduction with arm flexion. ● CTA brain/ EEG Thrombocytopneia ● Platelets survive 7-10 days (33% of them in spleen) ● Bleeding post op - <50,000 ○ If below 50,000 do NOT give DVT prophylaxis (do not give heraprin) ● Spontaneous intracranial bleed (<10,000) ● Causes ○ Drug induced (H2 blocker, HIT, Abx like Zosyn and Vanco) ○ Sepsis (Consumption) ○ Massive bleeding ○ TTP/HUS/DIC DVT Prophylaxis ● ● ● ● Indications: CHF, Severe respiratory disease, confined to bed, active cancer, sepsis, previous VTE, active neurologic disease, inflammatory bowel disease Types ○ Heparin - Metabolized in liver - (Do NOT give with liver failure) ○ Lovenox - Metabolized in kidney (watch GFR) (Do NOT give to renal failure patients) ■ Preferred because once a day and better in malignancy ⇒ Better for cancer patients ■ Dose adjust for malignancy Contraindications ○ Chemoprophylaxis: Bleeding, thrombocytopenia (<50,000) ○ TEDS/SCDs (sequential compression devices ■ Cause compression of the lower extremity veins. ■ CId with open wounds or DVT Reversal agent: Protamine sulfate Transfusions ● TRALI ○ Acute lung injury during or within 6 hours if administration ○ Hypoxia, pulmonary infiltrates on X-RAY, pink/frothy airway secretions, fever, hypotension ○ HYPOTENSION ○ Treatment: Discontinue infusion, BiPAP/Intubate ● TACO ○ HYPERTENSION ○ Volume overload, elevated BNP, hypertension ○ Treatment: Diuretics, BiPAP ● Hemolytic transfusion reaction – fevers and chills with respiratory distress (ABO incompatibility) ● Anaphylaxis – more stridor, cough, wheezing, rash ● If any of these rxn occur, the transfusion needs to be stopped immediately and the blood bank needs to be notified HIT - Normal INR ● Greater than 50% drop within 5-10 days of heparin exposure ● From IgG to platelet factor 4 ○ 4 Ts Score - DX ■ Thrombocytopenia ■ Timing, Thrombosis ■ Other cause of possibleThrombocytopenia ● Causes thrombocytopenia and prothrombotic state ● Discontinue heparin, HIT ELISA assay, Serotonin release assay ○ Serotonin release Assay is definite but takes several days ● Treat with Argatroban immediately if high suspicion Hematologist Conditons ● TTP ⇒ Normal INR - DOES NOT AFFECT INR ○ Pentad ■ Thrombocytopenia ■ Anemia ■ AMS ■ AKI ■ FEVER ○ Clinical diagnosis with CBC, peripheral smear, LDH, LFTs, Coags, +/- ADAMTS13 - Predcits likely hood of TTP ○ Plasma exchange therapy and steroids ● DIC - HIGH INR ○ Activation of coag cascade – prothrombotic state and depletion of fibrin and platelets ■ Bleeding + Clotting ■ Decrease Fibrin ○ Secondary to trauma/sepsis/malignancy ○ Elevated PT/aPTT/INR and decreased fibrin ○ Peripheral smear (Schistocytes) ○ Supportive care, transfuse if necessary, may need Cryoprecipitate ● HELLP – Hemolysis, Elevated LFTs, Low Platelets ● Uremic bleeding – Uremia causes platelet dysfunction, normal PT/PTT, elevated BUN ○ Treatment: HD DDAVP/Desmopressin Drugs/Treatments Substance S/S Diagnosis Treamtent Opioids Sedation/hypercarbic resp failure Mostly clinical. Urine drug tox Naloxone bolus vs gtt Acetaminophen Asymptomatic, N/V, Liver Failure Serum Acetaminophen levels Activated Charcoal if ingestion is less than 4hrs PTA Salicylates Abd pain, N/V, Metabolic Acidosis (MUDPILES) Salicylate Level Alkalization of the urine, HD Tricyclic Antidepressants Anticholinergic toxidrome -Mad as a Hatter/Red as Beet/ Blind as a Bat/Dry as a Bone/ Hot as a Desert Prolonged Qtc and TCA use hx IV sodium bicarbonate/ Physostigmine Bet Blockers Bradycardia/ hypotension Clinical Dx Atropine, Glucagon, cardiac pacing, ECMO Calcium Channel Blocker Bradycardia/ hypotension Clinical Dx Calcium Chloride Cocaine Hypertension/ Tachycardia Clinical hx, urine drug screen Benzos/Anti HTN (except for BB) – Nitroglycerin/Nitroprusside Cocaine causes excitement of both the alpha and beta receptors; BB will only block the Beta receptors. Nitroprusside S/S of cyanide toxicity: Tachycardia/confusion/tachypnea Treatment: Hydroxocobalamin and sodium thiosulfate (especially in renal failure) Benzodiazepine S/S: Sedation/hypercapnic resp failure Dx: Pmhx ?Suicide Note Tx: Flumazenil Thyroids Disorders Thyroid Disorder S/S Labs Treatment Hyperthyroidism ● ● ● ● ● Heat intolerance Weight loss Sinus tachycardia/Afib DTR +3 Thyroid Storm ○ Delirium ○ Hyperthermia ○ Graves Ds ● ● ● Low TSH Elevated T3 + 4 Amiodarone induced hyperthyroidism? ● ● ● Propylthiouracil (PTU) BB Steroid Therapy Hypothyroidism ● ● ● ● ● Hypotension Bradycardia Myxedema DTR-2 Hashimoto ds ○ Iatrogenic from radioactive iodine or surgery ● ● Elevated TS Low T3,4 ● Replacement/Supportiv e Endocrine Anterior ● HGH – Human Growth Hormone ○ Increases Ca++ retention and mineralization of the bone ○ Promotes lipolysis and protein synthesis ○ Gigantism vs acromegaly ● TSH- Thyroid Stimulating Hormone ○ Promotes the formation of T3/T4. ○ T3 is more active compared to T4. ● ● ● ● ○ Active thyroglobulin increases metabolism and aides with growth and development. ACTH – hormone that is released during stress states. Increases the production of cortisol by the adrenal cortex. Addison’s vs Cushing’s syndromes Prolactin – production of milk and helps with ovulation FSH – follicle stimulating hormone LH – luteinizing hormone Posterior ● ADH – Antidiuretic Hormone ○ Increases water reabsorption via the kidneys and causes vasoconstriction in the peripheral vasculature. ○ Vasopressin also increases Na in the serum transiently: SIADH vs DI ● Oxytocin ○ Found with contraction of the uterus with childbirth ○ Production of breast milk, and ejaculation of sperm Diabetes ● Diabetes Insipidus (DI) ○ Does not directly involve the pancreas or insulin production. ○ DI is due to deficiency or resistance of vasopressin (ADH). ○ Extreme polydipsia and polyuria. ○ Dx 24hr urine collection. >2L ■ Vasopressin Challenge Test ○ Treatment – Desmopressin ● Diabetes Mellitus (DM) ○ lack of production of insulin = Type 1, or production of ineffective insulin = Type 2. ○ Patients will present in a similar fashion as DI with polydipsia and polyuria but will have elevated blood glucose levels. ○ Dx – Blood Sugar/ A1C ■ C Peptide Test: Check to see if a patient has had synthetic insulin ○ Treatment – Insulin/Metformin ■ Metformin - Not preferred in ICU ⇒ Type B2 Lactic Acidosis DKA/HHNK DKA ● ● ● ● ● ● ● ● Usually type 1 Blood sugar >250, gap acidosis, ketones Nausea/Vomiting/Ab pain/Kussmaul ○ Do NOT Give DKA patients opioids (decrease gastric motility) Pseudohyponatremia!! ○ First think to do with DKA patient is check what their REAL sodium is! IV hydration and obtain frequent BS ○ Change to D5 once glucose <250 Insulin gtt, Monitor potassium ○ Potassium goes inside cell, risk of cardiac arrest ○ 3.0 K - Give Add longer acting insulin (Lantus), prior to the d/c of insulin gtt to prevent rebound hyperglycemia Goal is to decrease blood glucose levels by 50-100/hr to prevent encephalopathy HHNK ● Usually type 2 ● Higher blood sugars, more diuresis, more fluids needed ● Commonly seen with elderly who have poor PO intake/chronically ill Fever - Non-Infectious Causes ● Subarachnoid hemorrhage, Mesenteric ischemia, Heat stroke, Hyperthyroidism, Adrenal insufficiency, Malignant hyperthermia (NMS/SS), Acute alcohol withdrawal, Seizures, DVT/PE, Medications, blood products, Malignancy ● 5 W’s of Post Operation Fever ○ Wind – Atelectasis most likely the cause within the first 24-48hrs ■ Pain control + Spirometry ○ Water – UTI ○ Walk – DVT ○ Wound - infx ○ Wonder – Rx Infection of The CNS Meningitis – inflammation of the meninges surrounding the brain and spinal cord ● Triad ○ Fever ○ Stiff Neck ○ AMS ○ Treated empirically with abx and antivirals until confirmed negative. ● Head CT vs Spinal Tap ● Kermit and Brudzinski Sign ● Treatment - “Although receipt of abx prior to lumbar puncture will decrease the sensitivity of cx, abx tx should not be delayed to increase cx yield” ○ 1st - Give Steroids ⇒ Dexamethasone ○ 2nd - Give antibiotics ● Two most common community acquired pathogens = H influenza (children and young adults exp if not vaccinated) and N meningitides (rash) (which can be spread through air droplets). ● Strep pneumoniae should be considered for the middle aged ● Nosocomial meningitis = Staph Aureus. ● Viral meningitis = HSV/Enterovirus ● Treatment: Vanco + Ceftriaxone + Acyclovir. ○ Ampicillin should be given to pts 50 + to cover for listeria Burns ● ● ● ● Should calculate the percentage and the degree of surface area that is burned. Followed by using the Parkland formula to help with rapid fluid resuscitation. Lactated Ringers should be used instead of NSS due to the risk of hyperchloremic metabolic acidosis. Only 2nd and 3 rd degree burns should be considered with the parkland formula Parkland 9s ● ● ● First Degree – erythematous base with no bullae formation. Burn only to the epidermal layer usually found with sunburn. Second Degree (Partial thickness)- + bullae formation. Burn extends to the dermal layer. May need skin grafting depending on % Third Degree (Full thickness)– burn extends to the muscle layer + eshar. Burned area is usually painless due to damage to the nerves. Requires debridement of burned area along with muscle flaps Subarachnoid Hemorrhage ● ● ● ● ● ● ● ● Trauma is the most common cause but can be 2/2 to AVM. Headache is usually described as sudden and abrupt. Usually described as the worst headache of their life. “Thunderclap” May have N/V +/- LOC or focal deficits. Head CT should be obtained. If + bleed ⇒ Control Bp, sbp less than 160 to help prevent rebleeding Reverse coag (plt >50k, INR less than 1.4) and Consult NeuroSurg for possible stenting. ○ + Seizure control until aneurysm is secured, avoid phenytoin. ○ Control of nausea and vomiting. ○ Limit Valsalva stimuli prevents rupture. LP = RBC in spinal fluid +xanthochromia of CSF – heme breakdown products/ bilirubin. ○ Openingpressers will be elevated. If traumatic LP only RBC will be elevated, there will be no xanthochromia Subdural Hematoma ● Usually associated with traumatic event MVA/Fall/ assault,but can be 2/2 to infx. ● Blood gathers between the inner layer of the dura mater of the meninges. ● Bleeding usually results from tears in the bridging veins. ● SDH can cross sutural margins but is limited by dural attachments and therefore appears to be crescent shaped ● Signs and Symptoms ○ Loss of consciousness/irritability ○ Seizures pain/numbness ○ Headache/dizziness/nausea and vomiting. ○ Symptoms gradually increase as the bleeding worsens. ● Surgical intervention is required if bleed is greater than 10mm or midline shift of 5mm on initial brain scan. ● +/- Seizure ppx. Steroids should be avoided. ● Risk factors for hematoma expansion include: older age >65, hx of CAD, antithrombotic rx, AMS during examination, SDH associated with additional intracranial injuries, larger SDH volume, presence of intraventricular hemorrhage. Epidural Hematoma ● ● ● ● ● ● Associated with traumatic event. Mostly likely an arterial bleed. Bleeding between the skull and inner meningeal layer of the dura mater. More likely associated with young adults mean age 20-30s. EDH does NOT cross sutural margins but does cross dural attachments because its is located in the space between dura and skull. Signs and Symptoms ○ AMS ○ HA, vomiting, confusion ○ Hemiparesis ○ Some pts with acute edh have transient loss of consciousness have a “lucid interval” with recovery of consciousness followed by deteriorate due to hematoma enlargement