ĐĎॹá>ţ˙ •—ţ˙˙˙“”˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙ěĽÁ7 đżObjbjUU "Ę7|7|K˙˙˙˙˙˙l¨¨¨¨¨¨¨ź2222 2ŹźŐ5śŘ2Ř2Ř2Ř2Ř2Ř2Ř2Ř2T5V5V5V5V5V5V5$‹6 Ť8pz5¨Ř2Ř2Ř2Ř2Ř2z5¨4¨¨Ř2Ř25¨4¨4¨4Ř2*¨Ř2¨Ř2T5¨4Ř2T5¨4Ź¨4T5¨¨T5Ř2Ě2 0ŞşáŕXÁźX124ŚT5T5Ľ50Ő5T59¨49T5¨4źź¨¨¨¨Ů ACID / BASE #1 METABOLIC ACIDOSIS Winter's 1.5 (HCO3-) + 8 +/- 2 = Pa CO2 o Anion Gap acidoses: prodn: ketones, lactate ingestion: salicyllate, methanol, Et glycol elimination: renal failure, phosphates, sulfate prox tubule: HCO2- resorbtion dist tubule: H+ secretion, Aldo activity o Non AG: HCO3- matched by incr Cl- *GI tract loss( diarrhea, laxative, cholestyramine, CaCl2, MgCl2, ileal conduit *other: hyper PTH, diamox o RTA Prox: Urine pH often > 5.5 also see problems with other substances handled by prox tube ( glucose, AAs) o Distal ph Always > 5..5 #2 METABOLIC ALKALOSIS o Chloride sensitivie: (vomiting , NG tubes , hypovolemia--kidney tries to minimize HCO3- and Na losses, diuretics, villous adenoma (KCl diarhea), post hypercapnic (overshoot alkalosis), -urine Cl- < 20 meq/L o Chloride resistant -mineralocorticoid excess (Na resorbed, H out, volume expanded) -re-feeding. Ketones and lactae metab. to HCO3- - post oraganic aciosis, similar to refeeding, worse if HCO3- given o ANALYTIC METHODSo compare HCO3- and d Anion gap. If same, simple dissorder. If dHCO3- is less than d AG, then maybe a mixed Alk / Acidosis - hypoalbunimeia may obscure an otherwise wide anion gap. BE; change in acid/ base ( in nM) of whole blood needed to restore plasma pH to 7.4 at a pCO2 of 40mmHg. Anion gap: main value is in identifying a combined chronic resp acidosis + acute metabolic acidosis. ANTIDOTES Acetaminophen: Antidote - Acetylcysteine Dose - 140 mg/kg PO Arsenic, Mercury, & & Gold Antidote - BAL Dose - 5 mg/kg IM Atropine Antidote - Physostigmine Dose - 0.5 to 2.0 mg/kg Benzodiazapines Antidote - Flumazenil Dose - 0.2-1 mg IV Carbon Monoxide: Antidote - oxygen Cyanide: Antidote - Amyl nitrite Pearls q2min then Sodium nitrite 10 ml of 3% sol over 3 mins IV Ethylene glycol & Methanol: Antidote - Ethyl alcohol Dose - 1 ml/kg of 100% in glucose then dialysis Iron Antidote - Deferoxamine Dose - 40-90 mg/kg B-Blockers Antidote - Glucagon Dose - 5 mg/hr infusion Calcium channel blockers Antidote - Calcium chloride Dose - Bolus 60 mmol over 30 mins Lead Antidote - Calcium disodium versanate Dose - 1 amp/250 D5W over 1hr Methemoglobin Methylene blue 2mg/kg Nitrites Antidote - Methylene blue Dose - 0.2 ml/kg of 1% soln over 5 min Narcotics Antidote - Naloxone Dose - 0.4 to 0.8 mg Organophosphates Antidote - Atropine Dose - 0.5-2 mg and/or Antidote - PAM Dose - 1 g IV Aspiration recumbent: post segment of upper lobes upright: basal lower lobes *comm acquired: s. pneumo, s. aureus, H. influenza *hospitalized: GNR, psuedomonas, enterobactracae Treatment: recomended for those likely to have GI tract colonized (SBO, on PPI, etc.) and for those whose symptome do not resolve within 48 hrs. Evidence based criteria 1 randomizrd controlled, many IIa at least one RCT with comp. criteri IIb one RCT meeting some criteria III at lrasy one well-designrd trial without randomization IV opinions from authorities, case reports, etc, Fluid distribution (%TBW given) TBW- 0.60 of wgt - - - of this: 0.67 intracellular (40% wgt) 0.33 extracellular (20% wgt) , of ECFV: 0.25 vascular (5% wgt) 0.75 interstitial (15% wgt) Glascow Coma Scale •eyes open spont 4 to verbal 3 to pain 2 no resp 1 •best motor response obeys verbal 6 localizes pain 5 flexion withdrawl 4 flexion abnormal 3 extension 2 no response 1 •best verbal oriented, conversant 5 disorinted, convers. 4 inappropriate words 3 incomprehensible sounds 2 no response 1 gluccocorticoid potencies Gluccocorticoid (GC/ MC/ dose equiv) hydrocortisone 1 1 20 prednisone. - 4 0.8 5 solumedrol - 5 0.5 4 dexameth 25 0 0.75 betameth 25 0 0.6 Gram Stain Staph--GP clusers Strep--GPC occ rods Pneum--GP diplo, lancet, some chains Lactose fermenting: STRONG: E Coli, Enterobacter, Klebsiella WEAK: Citro, Providencia NOT: Proteus, Slmonella, Shig, Pseudo HYPEROSMOLAR NONKETOTIC DIABETIC COMA (HNDC) DESIGNATIONS: Also termed hyperosmolar coma, nonketotic hyperosmolar syndrome, and severe nonketotic hyperglycemic hyperosmolar syndrome. DEFINITION: HNDC is a state of extreme hyperglycemia, marked dehydration, serum hyperosmolarity, altered mental status, and absence of severe ketoacidosis (Ferri, 1991). The absence of severe ketosis distinguishes it from DKA. PROFILE: The patient is often a debilitated or elderly diabetic with impaired or no ability to communicate thirst over a 1-2 week period of osmotic diuresis. Event leading to relative insulin deficiency Hyperglycemia Osmotic diuresis Loss of large amounts of fluid and e'lytes (water loss > e'lyte loss) Prerenal azotemia (inability to excrete large amouts of glucose) Extreme hyperglycemia (avg glucose level: 900-1000 mg/dl) Hyperosmolarity (avg serum osmolarity is 380 mOsm/L) ETIOLOGY: It is important to identify a precipitating cause of HNDC. In a series described by Rippe (1992), causes could be found in 16 of 20 cases. 1. Infections: pneumonia, sepsis, UTI 2. Metabolic abnormalities: new DM, noncompliance 3. Cardiovascular: MI, CVA 4. Drugs a. Phenytoin and diazole: decreased insulin b. Diuretics: excessive dehydration c. Hypertonic alimentaion: osmotic diuresis PATHOPHYSIOLOGY: HNDC is relative insulin deficiency without ketosis. Pts have decreased levels of free fatty acids as compared with DKA. This supports the idea that there is sufficient insulin to prevent accelerated lipolysis characteristic of DKA which leads to ketogenesis and ketoacidosis. Ketone concentrations are elevated, however, to the starvation range: 2-4 mmole/L. Other possibilities include increased malonyl CoA production secondary to increased activity of the Cori cycle, where circulating glucose is converted to lactate in the liver for gluconeogenesis; from lactate comes malonyl CoA. Glucagon resistance may also contribute to decreased production of ketones. SYMPTOMS: Include polyuria, mental obtundation, SZ's, N/V. No acetone breath. PHYSICAL EXAM: 1. Dehydration signs: decreased skin turgor, dry mucous membranes, sunken eyes 2. Neural deficits: reversible hemiplegia, focal SZ 3. Orthostatic hypotension, tachycardia 4. Evidence of a precipitating factor LABORATORY: 1. Hyperglycemia: >600 mg/dl: often well over 1000 mg/dl 2. Hyperosmolarity 3. Na: may be low, normal, or elevated. More severe cases involve nl or high Na since serum Na has to be corrected when hyperglycemia occurs: for every 100 mg/dl increase in glucose above nl, Na is corrected 1.6 mEq/l, 2 mEq/l if there is accompanying dehydration. 4. K: low, nl, or elevated 5. HCO3: decreased (avg 17 mEq/l) 6. Avg pH = 7.26 7. Elevated BUN (60 - 90 mg/dl) 8. Decreased Ca, Mg, and P TREATMENT: 1.Vigorous fluid replacement 2. Replace electrolytes 3. Correct hyperglycemia a. vigorous hydration will decrease glucose 20 /hr b. Insulin, 2-5 U/hr by IV 4. Treat precipitating causes 5. Monitor vitals, e'lytes, U. O., mental status changes, insulin infused, and fluids administered. Infections after BMT 0-30 days- risk factor= neutropenia. Fungal and bacterial pneumonias, HSV, candida, Gram pos and Gram neg bacteria 30-90 days- risk factor= acute GVHD + therapy. Interstitial pneumonias, CMV, aspergillus 90 days- 12 months- risk factor= chronic GVHD. Bacterial and respiratory virus pneumonias, VZV, encapsulated bacteria Prophylaxis in BMT patients: 1) PCP- TMP/SMX from engraftment x3-6 mos when ANC>1000 OR if chronic GVHD as long as immunosuppressants given. Alternative: aerosolized pentamapine 2) fungal prophylaxis- consider fluconazole or low-dose ampho B. Fever and neutropenia x3-5 days without response to broad-spectrum abx should get ampho (0.5-1 mg/kg/d) 3) CMV- a) allo, CMV (-) donor & recipient, strict CMV (-) blood products- no prophylaxis b) allo, CMV (+) donor or recipient: IVIG (500 mg/kg q2wx3 mos) PLUS blood, urine, throat cx qwk x 120d. (+) cx- ganciclovir + gamma globulin c) autologous and (-) recipient- use (-) blood products. Liver--misc serum-ascites albumin gradient: >11g/dl--portal htn, sterile cirrhotic, liver mets, CA < 11g/dl TB, peritonitis, carcinomatosis of perit. SBP: <10g/dl incr risk prot <1g/dl, > 250 neutros/ml, low glu, high LDH, low pH ABD Tap: cell count, prot, alb, Cx, LDH, gram stain LP rbc wbc ratio --800/1 Mental Status Exam Appearance Behavior Attitude Speech quantity rate rhythm Mood fluctuation Affect range depth app. labile TP coherence direction distractability LOA FOA Impairments TC theme preocc. T.ins, broad, extr Hallucinations Abstraction Information Intellegence Concentration Cognition Orientation Memmory immed recent past past remote Judgment impulsive influences Insight Reliability Neurologic syndromesoo GBS--autoimmune demyelination.. Differential Lyme Dz if hypercellular CSF consider SC compression if B/Bl involved and paresis does not ascend Common Findings: ascending motor weakness limb numbness paresthesias facial 40% loss of DTR Less Common: bulbar invovement EOM Rare: Bladder Lab: incr CSF prot, v. few cells; Nosocomial Infections Epidemiology UTI 5-11/ 1000 catheter days Surgical 37% of all VAP (33%) 7-29/ 1000 days Catheter 5-15/ 1000 cath days Blood *coag neg. staph * s. aureus * enterococcus * candida Early Pneumonia * pneumococcus * MSSA * kelibsiella * enterobacter Late Pneumonia * pseudomonas * MRSA * acinetobacter * ressitant enterics UTIs * E. Coli * enterococcus * P. aerigunosa * GNR Surgical Wound * enterococcus * Coag neg. staph * enterobacter * pseudomonas OGELVIES --really only Lg bowel involved Inflamatory pancreatitis cholecystitis IBD radiation colitis Infectiou HSV SBP Ischemic IMA insufficiency Retroperitoneal neoplasms bleeding Reflex inhibition trauma choli urologic operations C-S neostigmine 2mg (NEJM 341: 192; 341: 1622, 1999) Pulm function 1 Pulm function o VC of 3X Vt needed for good cough o Lung resection; FEV1 < 800 mL prob and absolute contra to lung resection o PA balloon test: if mPAP > 40, PaO2 < 60, Pa CO2 > 45, likely RV falure or resp failure Pulm function 2 plasmapharesis or IVIG, no better with steriods intubate if VC < 15ml/kg or trending that way Poor prognosis: age > 60 full progression to intub in < 7 days decr motor amplitude on EEG complications delay in treatment Myesthenia Gravis occular, bulbar Rx: corticosteriods plus plasma exchange > IVIG look for related autoimmune pathology: Thyroid, adrenal, etc. Cholinergic Crisis::SLUDGE salivation lacrimation urination defication GI cramps emesis pinpoint pupils, wheezing, badycardia, coma Cirtical Illness Polyneuropathy: Thought secondary to SIRS, has both mmotor and sensory components, and can last for months Acute quadraplegic neuropathy: Motor only, secondary to NMBA, steriods, cn also have a myopathic component oPost Cardiac Arrest (hypoxic ischemic) injury Prognosis: presence of 4 risk factors on day 3 of coma predicts 96% mortality at 2 months: Abnormal brainstem fx (any test) No w-d to pain No verbal response Creatinine level > 1.5 mg/dl age > 70 o Skin Infections impetigo skin ecthyma erysipelas cellulitis sup faschia Nec Faschitis sub Q --> deep faschaial plane 1) fulminant with cutaneous exudate and hemorrhage 2) invisble with either anesthesia, or pain exceeding physical findings. Horizontal blood vessels not disupte Time of surgerry mortality < 24 hrs 6% > 24 hrs 25 % MRI T2 may is great at differentiating cellulitis vs. Nec Fash, but it should not delay surgical exploration if suspicion exists Radiocontrast • 0.45 NaCl 1ml/ kg/ hr for 12 hrs before and 12 hrs after procedure • N-acetyl cysteine 600 mg PO bid day before and day after procedure + NaCl as above. all protocols encourage to drink if thirsty Ramsey Sedation Scale 1 anxious, agitated, restless 2 cooperative, tranquil 3 responds to comands 4 asleep but brisk response to voice or glabellar tap 5 asleep, sluggish resp to stimuli 6 asleep, no response Seiz control undeirlying establish cv resp stability look for rhabido hyperthermia dehyd acidosis arrythmia pathophys incr CVP PAP MAP 25-30 min later you get cmro2 cbf mismatch w/decr oxygen delivery to cytochrome system. Excitotoxic fx then become problema tic Skin rash and pressure ulcers Drug rash: 1) morbilliform, cephalocaudal progression 2) erythema multiforme: target lesions, central bulla or necrotic center; if oral involvement, it's Stevens johnson. 3) Toxic epidermal necrolysis: extensive epidermal loss (sulfonamides, PCN, anticonvulsants) 4) vasculitis Life threateening Dissorders: 1) Purpura fulminans-- hemorrhagic infarction and necrosis of large areas of the skin, cause is unknown but is related to infections and disturbances in clotting 2) Ecthyma gangrenosum (pseudomonal infs.)Roundm indurated red to purpoe macules or plaques, cellulitis Pressure ulcer risks: physical and mental illness, age, bowel or blad incont., Best Rx: moist wound care, surg. consultation if III, IV Stroke **presentation **risk Stroke 9% for 5 years TIA 10% for first year 6% for each sub. year Asymptomatic soft plaque (high) 10% per year Ulcerated Plaques 7.5% per year Temp Regulation and Clinical Syndromes #1 Radiation: can take place in a vaccuum; heat can be absorbed, transmitted, reflected. Temp loss dT4. Undraped pt. #2 Convection: fluid motion - #3 Evaporation: predom. mode when T > 37C. #4 Conduction: 2 bodies in contact > 35 hypothermic 32-35 mild (incr HR, resp, diuresis, shiverrring, dMS) 28-32 mod (decr CO, ventilaiton, CNS, loss of shiv) < 28 severe (arrryth, p. edemma, circ. collapse) Heat exhaustion Heat stroke (HE + CNS dysfunction) exertional--exerc. w/ high temp, humidity classic--prro thermoreg. cannot cool self NMS (bromocryptine 2.5-7.5 po q8, Dnatrolene) Transfusion reactions *Febrile reactions: donor WBC react with pt. serum (leukoagglutanins) (1/1-200) *Allergic: mild (1/33-100) *IgA deficient have anti-IgA antibodies *Volume overload (1/100) *Acute lung injury: donor Igs react with host WBC, the opposite, or donor cytokines (1/5,000) *Deaths 80% ABO incompatible (1/12-33,000) 15% from ALI *Infectious/ septic (1/2000-20,000 for platelets) Vasculitis Small Vessel skin only--benign leukocytoclastic angiitis skin plus visceral involvement Henoch-schonlein purpura Mixed cryoglobulinemia assoc with conn tiss dz, malig. hypocomplement vasculitis involving the panniculus erythema nodosum weber-christian disease Medium sized vessels skin only livedo reticularis subcutaneous nodules systemic illnesses polyarteritis nodosum allergic granulomatosis (Churg Strauss) Wegeners lymphamatoid granulomatosis Large vessel vasculitis takayasus arteritis giant cell, polymyalgia rheumatica assoc with spondyloarthropathies Vitamins and Neuropsychatiric Syndromes Water-soluble vitamins: Coenzymes and prosthetic groups of enzymes involved in intermediate metabolism (see diagram). NIACIN (NAD, etc; many enz.) Endogenous production from Trp. Primary def: Corn-based diet Secondary Chronic EtOH; Isoniazid (see B6 below) Diagnosis: Urinary metabolites using HPLC Pathol: Motor neuron damage, dorsal column degeneration 1. early def: decr. appetite, wgt loss, decr. conc'n, abd. aches 2. inter " : irritability, depression/fatigue, insomnia 3. advanced (pellagra )dementia, dermatitis, diarrhea, death psychosis : mania, depression, delirium, paranoia, disorientation, confusion encephalopathic syndrome: clouding of consciousness, cogwheel rigidity, uncontrollable suckling and grasping reflexes B6, PYRIDOXINE (transaminases, conversion of Trp---> Niacin) Deficiency: Poor GI absorption Complexes with Isoniazid, Hydralizine. Penicillamine; incr. physical activity, pregnancy S/Sx: Weakness, irritability, seizures, periph. neuropathy, convulsions B1 THIAMINE (HMP shunt, entry into Krebs, a-KG--> Succinate) Uptake: folate dependent Storage: skeletal muscle Deficiency: Chronic EtOH ER Dose: 50mg IV, 50mg IM/day 1. Early: weakness, neuropathy, headache, tachycardia 2. Late: wet beriberi (CV) high output heart failure dry beriberi (Neural) 1. PNS: symmetrical decr. in motor, sensory and reflexes +/- parasthesias; legs involved > arms 2. CNS: Wernicke's syndrome ataxia opthalmoplegia H-nystagmus global confusion, apathy Korshakoff's psychosis: impaired memory ---> amnesia confabulation B2 RIBOFLAVIN (FAD, FMN; many enz., redox reactions, MAO) Sx: Personality deterioration Dermatitis, glossitis Retarded intellectual development Dx. RBC Glutathione reductase Conversion of B2 to FMN (flavokinase) inhibited by a number of common medicines: chlorpromazine, tricyclics, adriamycin B12 CYANOCOBALAMIN/ FOLIC ACID (DNA synth, methionine synth, FA synth/ myelin synthesis) Mental s/sx--frequent irritability apathy somnolence suspicious unstable depressive psychosis Dementia--rare presentation Peripheral NS (subacute combined degeneration of the spinal cord) : weakness, parasthesias--> unsteady gait--> stiff movements loss of vibratory sense, defecits are classically symmetrical-- asymmetry should make you consider other diagnoses Hematologic abnormalities: Manifestations of impaired DNA synthesis ***these will often follow CNS manifestations of vitamin deficiency, do not rule out B12 or folate deficiency because macrocytosis is absent !! Fat Soluble Vitamins: A variety of biochemical roles--antioxidant (E), light sensor (A), coenzyme (K), and hormone (D). Syndromes of hypervitaminosis are possible. Deficiency Excess A Night blindness Weakness, headache E Ataxia, peripheral neuropathy D Tetany Weakness, lethargy failure to thrive Trace minerals: Common prosthetic groups, enzyme cofactors Copper Excess (Wilson's disease) Neural S/sx: Dystonic facies, upper extr.; unsteady gait, tremor and loss of fine motor coordination, drooling, dysarthria Psychiatric: Intellectual deterrioration, personality changes, unstable behavior, routine tasks become difficult, organic dementia indistingusihable from bipolar or schizophrenia. Maganese deficiency Ataxia, convulsions Cromium deficiency (Cr complexes with nicotinamide to form "glucose tolerance factor," a factor required for proper binding of Insulin to its receptor). 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