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1- most probably cyctitis( supra pupic pain with burning micturation) however the other data pus cells,

crystals, proteins, are these RBCs normal or d ysmorphic,are needed to differentiate whether it's affecting upper or lower urin ary system. Infections, stones and autoimmune diseases are common causes for hea mturia at this age. Treatment will be given according to the cause whether antib iotics( quionlons are preferred), crystals disolvants according to it's type, th e patient may need further investigations on urinary system such as US.

2- Type2 Type2 Type2 diabetes can be prevented and can be treated without drugs only by exercis e and diet control

Type2DM IGT Impaired glucose tolerance silent IGT Micro and macrovascular complications IGT prevention type2 diabetes Polys atypical blurring of vision impotence Fasting>126 Postprandial>200 Random>200

prevention Screening of high risk groups Obese patient Patient with family history of DM ... Bad obstetric history (large baby,missed abortion,IUFD) 6 Fasting ,postprandial

postprandial 140199 IGT fasting 100125 IFGT DM .. IGT IFGT Wt reduction Exercise No caloric diet Drugs (insulin sensitizers ) insulin resistance They are antihyperglycemic not hypoglycemic drugs

metformin (glucophage,cidophage) glitazones Avandia,rosizone Primary prevention of type2 DM Type 2 diabetes is a syndrome and hyperglycaemia is one of its manifestations Obesity ,hypertension ,dyslipidemia,complications .

type2 diabetes IGT Fundus examination and follow up every year Lipid profile Urine analysis for microalbuminuria For early detection of nephropathy Repeated every6 months 20-200 microgm per min=microalbuminuria RF ECG To detect IHD as it may be silent

ACEI best line BBl

RF aldomet

liver CCB

type2 DM Fasting <140 Postprandial < 160 Eulipidemic Not hypertensive No microalbuminuria Life style modification is first line of treatment Diet control and exercise may be sufficient in ttt of type2 DM

Diet control and exercise may be sufficient in ttt of type2 DM Ketosis DIET Fine sugars 3 .... And proteins not encouraged as Only 15% And restrict proteins if there

before is renal or liver failure

20% fat avoiding saturated fatty acids Fast foods

EXERCISE

Oxygen Exercise? ( )

..... HDL Fibrinolytic activity Thrombosis Sensitivity of tissues to insulin ALL STRESSFUL SITUATION INCREASE NEEDS TO INSULIN EXCEPT EXERCISE Exercise 1 Start low and go slow Hypoglycaemia is more deleterious than hyperglycaemia ... 2 Biguanides (glucophage ,cidophage) Best antidiabetic .. Abdominal pain ,metallic taste ,diarrhoea Full dose 500

500 Side effects Hepatotoxic LCF HF ,corpulmonale Lactic acidosis Hypoxia

Decrease absorption of glucose from the gut Anorexigenic effect Hepatic glucose output .. 90 300 Circadian rhythm of antiinsulin hormones Not affect beta cells and so not cause hypoglycaemia Biguanides Sulphonylureas (diamicron,amaryl, ) Diamicron 806030 Start low and go slow Insulin sensitizers Avandia,rosizone,glitazone Beneficial for dyslipidemia Never produce hypoglycaemia

No side effects Contraindicated in hepatitis and HF as they cause salt and water retention .... Type2 DM ? 1. Failure of oral hypoglycaemics with full dose Oral 30 70 2. In LCF Ascetic , enzymes not high Oral 3. 4. ketosis

5. Glucophage ,amaryl in pregnant females Placenta Oral Pregnant Fasting ?95 Postprandial?126

: : it is ametabolic syndrome ending in hyperglycemia ending characterised by primary secondary

3-pulmonary embolism is not considered adisease but acomplication to an existing thrombus mostly DVT dDVT 1- SLOW CIRCULATION : varicose veins - obesity - heart failure -prolonged bed rest 2- HYPERCOAGULABILITY : congenital pregnancy postpartum polycythemia malignancy contraceptive pills dehydration 3- INDOTHELIAL INJURY ..

3 nephrotic syndrome Behcet syndrome sickle cell anemia

behcet sudden death this disease may be complicated by thrombophlebitis in the IVC causing thrombus leading to sudden death

unexplained ascites

acute liver failure : hypercoagulability encephalopathy

small size embolisem chest discom acute sudden attack of dyspnea, chest pain , shock and cyanosis in a predisposed pt recurrent embolizat thromboembolic pul hyperten mediam size chest pain pleuritic blood tinged sputum

minute RSHF PULMONARY HTN COR PULMONALE THEN RSH

massive embolise hypotension shock hypoxia acute right side fali

cyanosid perephra cyanosis of the tongue

: 3 PLEURETIC chest pain

tachypnoea tachycardia

4 : acute chest pain dyspnoea @ cyanosis shock acute cor pulmonale : 1- congested neck veins 2- tender liver

rapid distension of pul artery .hypoxia

tachypnea tachycardia in predisposed patient

ECG, CXR , D-Dimer, ECHO, spiral CT, V/Q scan , ABG ...

ECG >>> sinus tachycardia, AF, RV strain pattern , RBBB, S1Q3T3 , ST segment cha nges that could simulate MI sometimes

wedige area of pul infar pul oligemia pul edema pleur

......

respiratory alkalosis , hypoxia, that what I remembered !

spiral ct

: CT _angiography

pulmonary angiography invasive

3 : ABG : hypoxia & hypocapnea V\P scanning : perfusion is affected D . dimer

for the x-ray signs as mentioned by dr regional oligemia (Westermark sign): Dila of pulmonary vessels proximal to embolism along with collapse of distal vessels, often with a sharp cut off ... and (Hampton's) hump a pleural-based wedge shape d area of increased opacity

: MASSIVE lung collapse tension pneumothorax massive pulmonaery embolism massive pericardial effusion

1- : chest asymetry dullness on the collapsed side 2- : chest asymetry tympanetic resonance on the inflated side 3- : very distant heart sounds kaussmaul sign of neck veins

3 : pulmonary bronchial direct from air

: - - _ :

aortic dissection .

aortic dissection : 1- 2- .......

inspiration inspiratory fillg

Dont forget in suspicion of moderate to massive pulmonary embolism the role of e chocardiography ... findings of pulmonary hypertension and troponin .... positive results indicate severe RV dysfunction in appropriate ly suspected patients

HEPATO RENAL SYNDROME ______________________ ? Management Protocol Hepato-Renal Syndrome Definition 1 Hepato-renal syndrome is the development of renal failure in patients with sev ere liver disease in the absence of any identifiable renal pathology. 2 It is a functional rather than structural disturbance in renal function. The h istology of the kidney is virtually normal. Such kidneys have been successfully transplanted following which they functioned normally. After liver transplantati on kidney function also usually returns to normal. Diagnostic criteria - These are based largely on abnormal renal function tests, the absence of other causes of renal failure, and the absence of sustained improvement in renal func tion after diuretic withdrawal and fluid challenge. The presence of shock before deterioration of renal function precludes a diagnosis of hepato-renal syndrome. - Additional criteria describe the characteristics of urine flow and content, bu t since these may be present with other types of renal failure, for example acut e tubular necrosis, they are not considered essential for the diagnosis of hepat o-renal syndrome. in 1996 the International Ascites Club proposed diagnostic criteria for HRS Major criteria All of the following major criteria must be present : chronic or acute liver diseases with advanced hepatic failure and portal hyperte nsion. low-glomerular filtration rate, as indicated by serum creatinine of >1.5 mg/dL o r 24-h creatinine clearance <40 mL/min . absence of shock, ongoing bacterial infection, fluid loss, and current or recent treatment with nephrotoxic drugs. nosustained improvement in renal function (decrease in serum creatinine to 1.5 m g/dL or loss or increase in creatinine clearance to 40 Ml/min or more) following diuretic withdraw and expansion of plasma volume with 1.5 L of isotonic saline. proteinuria <500 mg/day. no ultrasonographic evidence of obstructive uropathy or parynchymal renal diseas e. Additional criteria These are frequently present in patients with HAS but are not necessary for diag nosis: urine volume >500 mL/24 h urine sodium > 10mmol/L Urine osmolality > plasma osmolality

urine red blood cells <50 per high-power field serum sodium concentration <130 mmol/L Clinical manifestations of HRS - HRS is classified as type-1 or type-2 according to both the intenisity and the manner of progression of renal failure. - These tow types exhibit different porognosis and survival rates, and each shou ld be treated differently. Type 1 HRS 1- Characterized by a severe and rapidly progressive renal failure defined as do ubling of the serum creatinine to a level greater than 2.5 mg/dL in less than 2 weeks 2- Patients usually have severe liver failure (jaundice, encephalopathy, and coa gulopathy) 3- Frequently occurs following a precipitating factor (severe bacterial infectio n, gastrointestinal haemorrhage, therapeutic paracentesis without plasma expansi on) 4- Is the complication with the poorest prognosis in cirrhosis? 5- Median survival time is only weeks Type 2 HRS I- Moderate and stable renal failure 2- Associated with relatively preserved liver failure 3- The main clinical consequence is refractory ascites 4- Median survival time is approximately 6 months

Investigation recommended: _______________________ serum creatinine urine analysis abdominal ultrasonography serum Na or urinary Na urine volume in 24 h Treatment __________ General measures --------------------Pharmacological treatment General measures 1-Measurement of the central venous pressure is important .Since renal dysfuncti on may be related to hypovolaemia. An intravenous fluid challenge is appropriate with up to 1.5 litre of saline or, if available, colloid such as human albumin solution 2 vials 2x50 ml. Monitoring the patient for fluid overload is necessary although this is not usually a problem because advanced cirrhosis have increase d venous compliance . 2-Potentially nephrotoxic drugs are stopped. 3-A search for sepsis is made. Ascites is tapped for white cell count, Gram stai n and culture. Blood, urine and cannula tips are cultured. A broad-spectrum anti biotic is started irrespective of proof of infection. 4-Tense ascites may be drained to improve renal haemodynamics by decreasing infe rior vena caval and renal vein pressure 5- The decision to use vasoconistrictor agents for HRS should be based on whethe r the patient is a realistic transplant candidate or if not, whether liver funct ion might be improve? 6- The only effective and permanent treatment for HRS is liver transplantation. Pharmacological treatment A. Duration of therapy: between 5-15 days.

B. Goal of therapy: reduction of serum creatinine below 1.5 mg/dl. C. Vasoconstrictors: The rational for use of these agents is to reverse the inte nse splanchnic vasodilatation, which is considered an important factor in ascite s formation and hepato-renal syndrome. Renal vasoconistriction reflects systemic and local responses to the reduced effective circulating volume. 1- Vasopressin Agonists ( expensive) . Ornipressin shorter half-life . Terlipressin (Glyopressin) longer half-life, fewer side-effect 2- Alternative long-term use of combination of both ( affordable choice) . ?-adrenergic agonists ( midodrine) . inhibitor of glucagons release ( octereotide sandostatin) D. Concomitant IV albumin infusion (1gm/kg on the first day, followed by 20-40 g m/day) should be administered to all patients. E. These drugs should be avoided in patients with cardiac diseases, peripheral a nd/or cerebrovascular diseases, duo to potential risk of ischemic events

Treatment of Type 1 HRS combination of both: ? ?-adrenergic agonists catecholamines (midodrine) . Midodrine 7.5 mg orally thr ee times daily with an increase to 12.5 mg three times daily if needed ? inhibitor of glucagons release octereotide (sandostatin) amp=0.1 mg ( 2 amp. of 0.1 mg sandostatin ampoule/24 h) by i.v. infusion for 24h. , or 0.1 mg sandosta tin subcutaneous three times daily with an increase to 200 microgram three times daily if needed. ? Concomitant IV albumin infusion (1 mg/kg on the first day, followed by 20-40 m g/day) should be administered to all patients. Treatment of type 2 HRS there are no studies evaluating the efficacy of treatment on renal function in p atients with type 2 HRS management is focused mainly on the treatment of refractory ascites, which is us ually found in these patients.

Prevention of HRS In three specific situations HRS may be successfully prevented ? Therapeutic paracentesis - Administration of plasma volume expanders, specifically albumin after total pa racentesis in patients with cirrhosis and ascites decreases the frequency of ren al failure and hyponatremia. ? Spontaneous bacterial peritonitis - Administration of albumin ( .5 g/kg iv. at the diagnosis of infection and I g/ kg iv. 48 h later) together with cefotaxime in patients with cirrhosis and spont aneous bacterial peritonitis markedly reduces the frequency of impairment in cir culatory function and the occurrence of type I HRS, ? Alcoholic hepatitis - The administration of the tumor necrosis factor inhibitor pentoxifylline (400m g t.i.d.) to patients with severe acute alcoholic hepatitis reduces the occurren ce of HRS

100 %

1- hepatorenal syndrome 2- hepatic &renal syndrome HRS

..... 1- IN HEPATORENAL : normal specific gravity of urine normal kidney size , shape & ecchogenicity 2- in hepatic &renal : specific gravity is low &fixed 1010 shrunken kidney with bad ecchogenicity 3 ....... 7

...... vasoconstriction of renal vessels .......... RAAS injury

: vasoconstrictors vasodilator

portal HTN >>splanchnic vasodilatation hepatorenal syndrome vasodilation HRS vasoconstrictors vasoconstrictoin in kidney

vasopressor when mean arterial blood pressure less than 75

HRS Liver transplantation hepatic &renal syndrome

HRS acute pre renal failure hypotentio

vasodi vasodilator or vasovonstrictor

.... acute pre renal failure

Jun

HRS vasocostriction of renal vessels vasodilation hypotention RAAS System vasoconstriction

........... ...

6 10

total paracentesis ?

Hepatic encephalopathy

---------------------> Acetaminophen Overdose ----------------------------1.Admit to: ------------- Medical intensive care unit. 2.Diagnosis: --------------- Acetaminophen overdose 3.Condition: --------------Patient appears: conscious- comatosed- semicomatosed- shocked- canosed- distres sed- pale. 4.Vital Signs: --------------- q1h with neurochecks. - Call physician if . BP >160/90, <90/60; . P >130, <50 <50; . R>25, <10; . urine output <20 cc/h for 3 hours. 5.Activity: ----------- Bed rest with bedside commode. 6.Nursing: ------------ Inputs and outputs, aspiration and seizure precautions. - Place large bore (Ewald) NG tube, then lavage with 2 L of NS. 7.Diet: -----NPO 8.IV Fluids: ----------9.Special Medications: ? Activated charcoal 30-100 gm doses, remove vianasogastric suction prior to ace tylcysteine. ? Acetylcysteine (Mucomyst, NAC) 5% solution loading dose 140 mg/kg via nasogast ric tube, then 70 mg/kg via NG tube q4h x 17 doses

? ? ? ?

Complete all NAC doses even if acetaminophen levels fall below toxic range. Phytonadione (konakion) 5 mg IV/IM/SQ (if INR increased). Fresh frozen plasma 2-4 U (if INR is unresponsive to konakion). Trimethobenzamide (Tigan) 100-200 mg IM/PR q6h prn nausea.

10.Extras: ECG. 11.Labs: CBC, SMA 7&12, LFTs, INR/PTT, Acetaminophen level now and in 4h. UA.

(2) __________________ Acute Renal Failure ------------------------------?------------------------------?---------------------------Acute renal failure is defined as a sudden decrease in renal function sufficient to increase the concentration of nitrogenous wastes in the blood. It is charact erized by an increasing BUN and creatinine. I. Clinical presentation of acute renal failure ------------------------------?-------------------A. Oliguria is a common indicator of acute renal failure, and it is marked by a decrease in urine output to less than 30 mL/h. Acute renal failure may be oligur ic (<500 L/day) or nonoliguric (>30 mL/h). Anuria (<100 mL/day) does not usually occur in renal failure, and its presence suggests obstruction or a vascular cau se. B. Acute renal failure may also be manifest by encephalopathy, volume overload, pericarditis, bleeding, anemia, hyperkalemia, hyperphosphatemia, hypocalcemia, a nd metabolic acidemia. II. Clinical causes of renal failure ------------------------------?------A. Prerenal insult -------------------1. Prerenal insult is the most common cause of acute renal failure, accounting f or 70% of cases. Prerenal failure is usually caused by reduced renal perfusion s econdary to extracellular fluid loss (diarrhea, diuresis, GI hemorrhage) or seco ndary to extracellular fluid sequestration (pancreatitis, sepsis), inadequate ca rdiac output, renal vasoconstriction (sepsis, liver disease, drugs), or inadequa te fluid intake or replacement. 2. Most patients with prerenal azotemia have oliguria, a history of large fluid losses (vomiting,diarrhea, burns), and evidence of intravascular volume depletio n (thirst, weight loss, orthostatic hypotension, tachycardia, flat neck veins, d ry mucous membranes). Patients with congestive heart failure may have total body volume excess (distended neck veins, pulmonary and pedal edema) but still have compromised renal perfusion and prerenal azotemia because of diminished cardiac output. 3. Causes of prerenal failure are usually reversible if recognized and treated e arly; otherwise, prolonged renal hypoperfusion can lead to acute tubular necrosi s and permanent renal insufficiency. B. Intrarenal insult --------------------1. Acute tubular necrosis (ATN) is the most common intrinsic renal disease leadi ng to ARF. a. Prolonged renal hypoperfusion is the most common cause of ATN.

b. Nephrotoxic agents (aminoglycosides, heavy metals, radiocontrast media, ethyl ene glycol) represent exogenous nephrotoxins. ATN may also occur as a result of endogenous nephrotoxins, such as intratubular pigments (hemoglobinuria), intratu bular proteins (myeloma), and intratubular crystals (uric acid). 2. Acute interstitial nephritis (AIN) is an allergic reaction secondary to drugs (NSAIDs, $-lactams). 3. Arteriolar injury occurs secondary to hypertension, vasculitis, microangiopat hic disorders. 4. Glomerulonephritis secondary to immunologically mediated inflammation may cau se intrarenal damage. C. Postrenal insult - Results from obstruction of urine flow. Postrenal insult is the least common c ause of acute renal failure, accounting for 10%. Postrenal insult may be caused by obstruction secondary to prostate cancer, benign prostatic hypertrophy, or re nal calculi. Postrenal insult may be caused by amyloidosis, uric acid crystals, multiple myeloma, methotrexate, or acyclovir. III.Clinical evaluation of acute renal failure ------------------------------?------------------A. Initial evaluation of renal failure should determine whether the cause is dec reased renal perfusion, obstructed urine flow, or disorders of the renal parench yma. Volume status (orthostatic pulse, blood pressure, fluid intake and output, daily weights, hemodynamic parameters), nephrotoxic medications, and pattern of urine output should be assessed. B. Prerenal azotemia is likely when there is a history of heart failure or extra cellular fluid volume loss or depletion. C. Postrenal azotemia is suggested by a history of decreased size or force of th e urine stream, anuria, flank pain, hematuria or pyuria, or cancer of the bladde r, prostate or pelvis. D. Intrarenal insult is suggested by a history of prolonged volume depletion (of ten post-surgical), pigmenturia, hemolysis, rhabdomyolysis, or nephrotoxins. Int rarenal insult is suggested by recent radiocontrast, aminoglycoside use, or vasc ular catheterization. Interstitial nephritis maybe implicated by a history of me dication rash, fever, or arthralgias. E. Chronic renal failure is suggested by diabetes mellitus, normochromic normocy tic anemia, hypercalcemia, and hyperphosphatemia. IV. Physical examination ---------------------------A. Cardiac output, volume status, bladder size, and systemic disease manifestati ons should be assessed. B. Prerenal azotemia is suggested by impaired cardiac output (neck vein distenti on, pulmonary rales, pedal edema). Volume depletion is suggested by orthostatic blood pressure changes, weight loss, low urine output, or diuretic use. C. Flank, suprapubic, or abdominal masses may indicate an obstructive cause. D. Skin rash suggests drug-induced interstitial nephritis; palpable purpura sugg ests vasculitis; nonpalpable purpura suggests thrombotic thrombocytopenic purpur a or hemolytic-uremic syndrome. E. Bladder catheterization is useful to rule out suspected bladder outlet obstru ction. A residual volume of more than 100 mL suggests bladder outlet obstruction . F. Central venous monitoring is used to measure cardiac output and left ventricu lar filling pressure if prerenal failure is suspected. V. Laboratory evaluation ---------------------------A. Spot urine sodium concentration 1. Spot urine sodium can help distinguish between prerenal azotemia and acute tu bular necrosis. 2. Prerenal failure causes increased reabsorption of salt and water and will man

ifest as a low spot urine sodium concentration <20 mEq/L and a low fractional so dium excretion <1%, and a urine/plasma creatinine ration of >40. Fractional excr etion of sodium (%) = ([urine sodium/plasma sodium] [urine creatinine/plasma cre atinine] x 100). 3. If tubular necrosis is the cause, the spot urine concentration will be >40 mE q/L, and fractional excretion of sodium will be >1%. B. Urinalysis 1. Normal urine sediment is a strong indicator of prerenal azotemia or may be an indicator of obstructive uropathy. 2. Hematuria, pyuria, or crystals may be associated with postrenal obstructive a zotemia. 3. Abundant cells, casts, or protein suggests an intrarenal disorder. 4. Red cells alone may indicate vascular disorders. RBC casts and abundant prote in suggest glomerular disease (glomerulonephritis). 5. White cell casts and eosinophilic casts indicate interstitial nephritis. 6. Renal epithelial cell casts and pigmented granular casts are associated with acute tubular necrosis. C. Ultrasound is useful for evaluation of suspected postrenal obstruction (nephr olithiasis). The presence of small (<10 cm in length), scarred kidneys is diagno stic of chronic renal insufficiency. VI. Management of acute renal failure ------------------------------?-------------A. Reversible disorders, such as obstruction, should be excluded, and hypovolemi a should be corrected with volume replacement. Cardiac output should be maintain ed. In critically ill patients, a pulmonary artery catheter should be used for e valuation and monitoring. B. Extracellular fluid volume expansion. Infusion of a 1-2 liter crystalloid flu id bolus may confirm suspected volume depletion. C. If the patient remains oliguric despite euvolemia, IV diuretics may be admini stered. A large single dose of furosemide (100-200 mg) may be administered intra venously to promote diuresis. If urine flow is not improved, the dose of furosem ide may be doubled. Furosemide may be repeated in 2 hours, or a continuous IV in fusion of 10-40 mg/hr (max 1000 mg/day) may be used. D. The dosage or dosing intervals of renally excreted drugs should be modified. E. Hyperkalemia is the most immediately life-threatening complication of renal f ailure. Serum potassium values greater than 6.5 mEq/L may lead to arrhythmias an d cardiac arrest. Potassium should be removed from IV solutions. Hyperkalemia ma y be treated with sodium polystyrene sulfonate (Kayexalate), 30-60 gm PO/PR ever y 4-6 hours. F. Hyperphosphatemia can be controlled with aluminum hydroxide antacids (eg, Amp hojel or Basaljel), 15-30 ml or one to three capsules PO with meals, should be u sed. G. Fluids. After normal volume has been restored, fluid intake should be reduced to an amount equal to urinary and other losses plus insensible losses of 300-50 0 mL/day. In oliguric patients, daily fluid intake may need to be restricted to less than 1 L. H. Nutritional therapy. A renal diet consisting of daily high biologic value pro tein intake of 0.5 gm/kg/d, sodium 2 g, potassium 40-60 mg/day, and at least 35 kcal/kg of nonprotein calories is recommended. Phosphorus should be restricted t o 800 mg/day I. Dialysis. Indications for dialysis include uremic pericarditis, severe hyperk alemia, pulmonary edema, persistent severe metabolic acidosis (pH less than 7.2) , and symptomatic uremia. ------------------------------?------------------------------?-------------------------<> /

Management Protocol of Cocaine poisoning ------------------------------?------------------Modes of action Blocks reuptake of dopamine (causing euphoria, hyperactivity) and noradrenaline (causing vasoconstriction and hypertension) Blocks Na+ channels, resulting in a local anaesthetic action and myocardial depr ession Platelet activation Complications - Chest pain related to myocardial ischaemia or infarction. Local chest pain gui delines should be followed. - ECG abnormalities often resolve within 12h. Arrhythmias should be treated conv entionally, though avoiding ?-blockers. - Heart failure from myocardial depression or a cardiomyopathy Seizures - Cerebrovascular accidents - Pneumothorax - Rhabdomyolysis - Premature labour abruption - Agitated delirium, hyperthermia - Thermal injury from smoke inhalation Management 1. Oxygen.

2. 3. 4. 5. 6.

Diazepam for agitation, delirium, chest pain. Aspirin for chest pain, CVA. Nitrates for chest pain, heart failure. Sodium bicarbonate and forced diuresis for rhabdomyolysis. ?-blockers should be avoided

------------------------------?--------------Management Protocol of Anaphylaxis 1.Admit to: -----------ICU 2.Diagnosis: -------------- Anaphylaxis 3.Condition: --------------Patient appears: conscious- comatosed- semicomatosed- shocked- canosed- distres sed- pale 4.Vital Signs: --------------- q1-4h; - call physician if: . BP systolic >160, <90; diastolic >90, <60; . P >120, <50; . R>25, <10; . T>38.5C 5.Activity: ---------- Bedrest 6.Nursing: ------------ O2 at 6 L/min by NC or mask. - Keep patient in Trendelenburg's position, - No. 4 or 5 endotracheal tube at bedside. - Foley to closed drainage. 7.Diet: ------- NPO 8.IV Fluids: ------------- 2 IV lines. Normal saline or LR 1 L over 1-2h, - then D5 1/2 NS at 125 cc/h.

9.Special Medications: ------------------------Immediate treatment with epinephrine is imperative. Epinephrine is an antagonist to the effects of the chemical mediators on smooth muscle, blood vessels, and o ther tissues. ? For mild reactions (eg, generalized pruritus, urticaria, angioedema, mild whee

zing, nausea, and vomiting), - 0.01 mL/kg aqueous epinephrine 1:1000 sc (usual dose 0.3 to 0.5 mL in adults) should be given. - If an antigen injected into an extremity caused the anaphylaxis, a tourniquet should be applied above the injection site and 1/2 of the above dose of epinephr ine also injected into the site to reduce systemic absorption of the antigen. - A second injection of epinephrine subcutaneously may be needed. After symptoms resolve, - an oral antihistamine should be given for 24 h. - Methylprednisolone (Solu-Medrol) 250 mg IV x 1, then 125 mg IV q6h OR Hydrocor tisone sodium succinate 200 mg IV x 1, then 100 mg q6h, followed by oral prednis one 60 mg PO qd, tapered over 5 days. ? For more severe reactions, with massive angioedema but without evidence of car diovascular involvement, - adult patients should be given diphenhydramine 50 to 100 mg IV in addition to the above treatment to forestall laryngeal edema and to block the effect of furt her histamine release. - When the edema responds, 0.005 mL/kg of an aqueous suspension of long-acting e pinephrine 1:200 sc (maximum dose, 0.15 mL) can be given for its 6- to 8-h effec t; an oral antihistamine should be given for the next 24 h. - Methylprednisolone (Solu-Medrol) 250 mg IV x 1, then 125 mg IV q6h OR Hydrocor tisone sodium succinate 200 mg IV x 1, then 100 mg q6h, ? For asthmatic reactions that do not respond to epinephrine, - IV fluids should be started, - and (if the patient is not on theophylline) theophylline 5 mg/kg IV can be giv en over 10 to 30 min, followed by 0.5 mg/kg/h, more or less, to maintain a theop hylline blood level of 10 to 20 g/mL (55 to 110 mol/L). - Albuterol (Ventolin) 0.5%, 0.5 mL in 2.5 mL NS q30min by nebulizer prn - Methylprednisolone (Solu-Medrol) 250 mg IV x 1, then 125 mg IV q6h OR Hydrocor tisone sodium succinate 200 mg IV x 1, then 100 mg q6h, - Endotracheal intubation or tracheostomy may be needed, with O2 at 4 to 6 L/min . ? The most severe reactions usually involve the cardiovascular system, causing s evere hypotension and vasomotor collapse. - IV fluids should be rapidly infused and the patient should be recumbent with l egs elevated. - Epinephrine (1:100,000) should be given slowly IV (5 to 10 g/min) with close ob servation for development of side effects, including headache, tremulousness, na usea, and arrhythmias. - The underlying severe hypotension may be due to vasodilation, hypovolemia from loss of fluid, myocardial insufficiency (rarely), or a combination of these. Ea ch reaction has a specific treatment, and often the treatment of one exacerbates the others. The appropriate therapy may be clarified if central venous pressure (CVP) and left atrial pressure can be measured. - ?A low CVP and normal left atrial pressure indicate peripheral vasodilation an d/or hypovolemia. Vasodilation should respond to epinephrine (which will also re tard the loss of intravascular fluid). - Hypovolemia is usually the major cause of the hypotension. The CVP and left at rial pressure are both low, and large volumes of saline must be given, with BP m onitored until the CVP rises to normal. Colloid plasma expanders (eg, dextran) a re rarely necessary. Only if fluid replacement does not restore normal BP should treatment be started cautiously with vasopressor drugs (eg, dopamine, norepinep hrine). - ?Cardiac arrest may occur, requiring immediate resuscitation . Further therapy depends on ECG findings. - When all the above measures have been instituted, diphenhydramine (50 to 75 mg IV slowly over 3 min) may then be given for treatment of slow-onset urticaria, asthma, laryngeal edema, or hypotension. - ?Complications (eg, MI, cerebral edema) should be watched for and treated appr

opriately. - Patients with severe reactions should be observed in the hospital for 24 h aft er recovery in case of relapse. - ?Those who had an anaphylactic reaction to an insect sting should carry and us e a pre-filled syringe of epinephrine for prompt self-treatment of any future re action. They should be referred for venom immunotherapy (desensitization). 10.Extras: ----------- Portable CXR, ECG 11.Labs: --------- CBC, ..............................?............... /

Management ProtocoL of Alcohol Withdrawal ------------------------------?----------------------1.Admit to: ------------ ICU 2.Diagnosis: --------------- Alcohol withdrawals/delirium tremens. 3.Condition: ---------------------Patient appears: conscious- comatosed- semicomatosed- shocked- canosed- distres sed- pale. 4.Vital Signs: ------------------ q4-6h. - Call physician if . BP >160/90, <90/60; . P >130, <50; . R>25, <10; . T >38.5C; or

. increase in agitation. 5.Activity: ---------------- Heparin lock or - D5 1/2 NS at 100-125 cc/h. 6.Nursing: ------------- Seizure precautions. - Soft restraints prn. 7.Diet: ------------ Regular, push fluids. 8.IV Fluids: --------------- Heparin lock or - D5 1/2 NS at 100-125 cc/h. 9.Special Medications: -------------------------? Withdrawal syndrome: -Chlordiazepoxide (Librium) 50-100 mg PO/IV q6h for 3 days OR -Lorazepam (Ativan) 1 mg PO tid-qid. ? Delirium tremens: -Chlordiazepoxide (Librium) 100 mg slow IV push or PO, repeat q4-6h prn agitatio n or tremor for 24h; max 500 mg/d. Then give 50-100 mg PO q6h prn agitation or t remor OR -Diazepam (Valium) 5 mg slow IV push, repeat q6h until calm, then 5-10 mg PO q46h. ? Seizures: -Thiamine 100 mg IV push AND -Dextrose water 50%, 50 mL IV push. -Lorazepam (Ativan) 0.1 mg/kg IV at 2 mg/min; may repeat x 1 if seizures continu e. ? Wernicke-Korsakoff Syndrome: -Thiamine 100 mg IV stat, then 100 mg IV qd. 10.Symptomatic Medications: -Multivitamin 1 amp IV, then 1 tab PO qd. -Folate 1 mg PO qd. -Thiamine 100 mg PO qd. -Acetaminophen (Tylenol) 1-2 PO q4-6h prn headache. 11.Extras: ------------ CXR, - ECG. - Alcohol rehabilitation and - social work consult.

12.Labs: ---------------- CBC, - SMA 7&12, - Mg, - amylase, - lipase, - liver panel, - urine drug screen. - UA, - INR/PTT. ----------------------- { /

... ------------------------------?---------

Management Protocol of Asthma ------------------------------?---------1.Admit to: ---------- ICU 2.Diagnosis: --------------- Exacerbation of asthma 3.Condition: ----------------Patient appears: conscious- comatosed- semicomatosed- shocked- canosed- distres sed- pale. 4.Vital Signs: -------------- q6h. - Call physician if . P >140; R >30, <10; . T >38.5C; . pulse oximeter <90% 5.Activity: -------------- Up as tolerated. 6.Nursing: -------------- Pulse oximeter, - bedside peak flow rate before and after bronchodilator treatments. 7.Diet: ---------- Regular, - no caffeine. 8.IV Fluids: ----------------- D5 1/2 NS at 125 cc/h. 9.Special Medications: -------------------------? Oxygen 2 L/min by NC. Keep O2 sat >90%. ? Beta-Agonists, Acute Treatment: -Albuterol (Ventolin) 0.5 mg and ipratropium (Atrovent) 0.5 mg in 2.5 mL NS q1-2 h until peak flow meter >200-250 L/min and sat >90%, then q4h OR -Albuterol (Ventolin) MDI 3-8 puffs, then 2 puffs q3-6h prn, or powder 200 mcg/c apsule inhaled qid. -Albuterol/Ipratropium (Combivent) 2-4 puffs qid. ? Systemic Corticosteroids: -Methylprednisolone (Solu-Medrol) 60-125 mg IV q6h; then 30-60 mg PO qd. OR -Prednisone 20-60 mg PO qAM. ? Aminophylline and Theophylline (second-line therapy): -Aminophylline load dose: 5.6 mg/kg total body weight in 100 mL D5W IV over 20 m in. Maintenance of 0.5- 0.6 mg/kg ideal body weight/h (500 mg in 250 Ml D5W); re duce if elderly, heart/liver failure (0.2-0.4 mg/kg/hr). Reduce load 50-75% if t

aking theophylline (1 mg/kg of aminophylline will raise levels 2 mcg/mL) OR -Theophylline IV solution loading dose 4.5 mg/kg total body weight, then 0.4-0.5 mg/kg ideal body weight/hr. -Theophylline (Theo-Dur) 100-400 mg PO bid (3 mg/kg q8h); 80% of total daily IV aminophylline in 2-3 doses. ? Maintenance Inhaled Corticosteroids (adjunct therapy): -Advair Diskus (fluticasone/salmeterol) one puff bid [doses of 100/50 mcg, 250/5 0 mcg, and 500/50 mcg]. Not appropriate for acute attacks. -Beclomethasone (Beclovent) MDI 4-8 puffs bid, with spacer 5 min after bronchodi lator, followed by gargling with water. -Triamcinolone (Azmacort) MDI 2 puffs tid-qid or 4 puffs bid. ? Maintenance Treatment: -Salmeterol (Serevent) 2 puffs bid; not effective for acute asthma because of de layed onset of action. -Pirbuterol (Maxair) MDI 2 puffs q4-6h prn. -Bitolterol (Tornalate) MDI 2-3 puffs q1-3min, then 2-3 puffs q4-8h prn. -Fenoterol (Berotec) MDI 3 puffs, then 2 bid-qid. -Ipratropium (Atrovent) MDI 2-3 puffs tid-qid. ? Prevention and Prophylaxis: -Cromolyn (Intal) 2-4 puffs tid-qid. -Nedocromil (Tilade) 2-4 puffs bid-qid. -Montelukast (Singulair) 10 mg PO qd. -Zileuton (Zyflo) 600 mg PO qid. ? Acute Bronchitis -Ampicillin/sulbactam (Unasyn) 1.5 gm IV q6h OR -Cefuroxime (Zinacef) 750 mg IV q8h OR -Cefuroxime axetil (Ceftin) 250-500 mg PO bid OR -Trimethoprim/sulfamethoxazole? (Bactrim DS), 1 tab PO bid OR -Levofloxacin (Levoxin) 500 mg PO/IV PO qd [250, 500 mg]. -Amoxicillin 875 mg/clavulanate 125 mg (Augmentin 875) 1 tab PO bid.

10.Symptomatic Medications: ------------------------------?-----Docusate sodium (Colace) 100 mg PO qhs. -Famotidine (Pepcid) 20 mg IV/PO q12h OR -Lansoprazole (Losec) 30 mg qd. -Acetaminophen (Tylenol) 325-650 mg PO q4-6h prn headache. -Zolpidem (Ambien) 5-10 mg qhs prn insomnia. 11.Extras: ------------- Portable CXR, - ECG, - pulmonary function tests before and after bronchodilators; - pulmonary rehabilitation; - impedance cardiography, - echocardiogram. 12.Labs: ------------- ABG, - CBC with eosinophil count, - SMA7, B-type - Theophylline level stat and after 24h of infusion.

- Sputum Gram stain, C&S. --------------------------- /

----------------------------Hypertensive Encephalopathy ------------------------------?-----1.Admit to: ------------ICU 2.Diagnosis: -------------Hypertensive emergencies Hypertensive Encephalopathy 3.Condition: --------------Patient appears: conscious- comatosed- semicomatosed- shocked- canosed- distres sed- pale. 4.Vital Signs: ---------------q30min until BP controlled, then q4h. 5.Activity: ----------Bed rest 6.Nursing: --------------Intra-arterial BP monitoring, daily weights, inputs and outputs. 7.Diet: -------Clear liquids. 8.IV Fluids: -----------D5W at TKO. 9.Special Medications: -------------------------? Nitroprusside sodium: This is the drug of choice in most hypertensive emergenc ies. It is a potent direct vasodilator which acts as a nitric oxide donor to red uce both the preload and the afterload. The dose ranges from 0.25-10 mcg/kg/min IV infusion (50 mg in 250 mL of D5W), The infusion is started at 15 g/mm and caut iously increased by 5-10 g/mm every 3-5 minutes until the desired blood pressure is reach .titrate to desired BP. The most common adverse reaction is hypotension . The physician should be extremely careful to avoid undesirable reduction of bl ood pressure. ? Nitroglycerin (Tridil- Nitrocin): This widely available direct vasodilator act s primarily by reduction of venous preload. However at high infusion rates, it a lso reduces the systemic vascular resistance. The dose ranges from IV infusion 2 0-150 g/mm. Because of its favourable effect on myocardial ischemia, it is partic

ularly effective in acute coronary syndromes and acute pulmonary oedema ? Labetalol (Trandate) 20 mg IV bolus (0.25 mg/kg), then 20-80 mg boluses IV q10 -15min, titrate to desired BP or continuous IV infusion of 1.0-2.0 mg/min, titra te to desired BP. Ideal in patients with thoracic or aortic abdominal aneurysm. ? Phentolamine [pheochromocytoma], 5-10 mg IV, repeated as needed up to 20 mg. ? Trimethaphan (Arfonad) [dissecting aneurysm] 2-4 mg/min IV infusion (500 mg in 500 mL of D5W). Practical Considerations ? Intravenous diuretics should not be used as initial therapy in a hypertensive crisis unless the patient presents in acute pulmonary oedema or cerebral oedema or there is evidence of extracellular volume expansion. -The haemodynamic profile of hypertensive crisis is characterized by a pronounce d elevation of systemic vascular resistance and volume depletion. -Intravenous loop diuretics will aggravate the hypovolaemia and further stimulat e renin-angiotensin activity which may exacerbate hypertension and cause further deterioration in renal function. -Oral diuretic therapy can be added for optimal long-term control of blood press ure after the acute stage of management. ? The practice of managing hypertensive crisis with a combination of a rapidly a cting sublingual nifedipine plus an IV loop diuretic should be avoided. The unco ntrolled reduction of arterial pressure using these drugs may result in organ hy poperfusion and catastrophic end-organ damage such as cerebral infarction, or ac ute myocardial infarction. ? Some physicians may not have hospital access to provide appropriate IV infusio n therapy; it is possible to allow the administration of a single dose of sublin gual captopril 12.5 mg (1/2 tablet of 25 mg) with close monitoring of blood pres sure until the patient can be transferred to a properly equipped hospital. The a ction of sublingual captopril starts in 30 minutes, peaks at 50 minutes and last s for 4-6 hours. -- It is not effective in all patients and is contraindicated i n patients with suspected bilateral renal artery stenosis and in pregnancy. Clon idine, alpha methyldopa (aldomet) can bring rapid reduction in blood pressure (w ithin three hours) after oral administration. 10.Symptomatic Medications: ------------------------------?----Acetaminophen (Tylenol) 325-650 mg PO q4-6h prn headache. -Zolpidem (Ambien) 5-10 mg qhs prn insomnia. -Zantak 150 mg PO. 11.Extras: -------------Portable CXR, ECG, impedance cardiography, echocardiogram. 12.Labs: ----------CBC, TSH, free T4, Plasma catecholamines, urine drug screen. ------------------------------?------------- /