 \200 ACUTE CORONARY SYNDROME (1) 389 Key papers Yusuf S for the Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. (2001) Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 345: 494 \200\223502. Task Force for Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of European Society of Cardiology. (2007) Guidelines for the diagnosis and treatment of no n- ST-segment elevation acute coronary syndromes. Eur Heart J 28: 1598 \200\223660. See also: Coronary revascularisation techniques, p104; ECG monitoring, p162; Echocardiograp hy, p192; Cardiac function tests, p216; Vasodilators, p266; Anti-anginal agents, p276; Acut e coronary syndrome (2), p390; Heart failure \200\224assessment, p392. 390 CHAPTER 23 Cardiovascular disorders Acute coronary syndrome (2) Diagnosis of myocardial infarction Rise and/or fall of cardiac biomarkers (preferably troponin) above upper reference limit plus evidence of myocardial is chaemia with \211 1 of: \200 \200 \200 \200 Symptoms of ischaemia. ECG changes of new ischaemia (new ST \200\223T changes or new LBBB). Pathological Q waves on ECG. New loss of myocardium or new regional wall motion abnormalit y. Management of uncomplicated infarction \200 \200 \200 Oxygen \200\224to maintain SaO2 \211 98%. Good venous access and continuous ECG monitoring . Appropriate and prompt monitoring plus investigations as indicated, e.g. echocardiography , angiography, cardiac output monitoring. Adequate pain relief. Aspirin. Urgent referral fo r percutaneous coronary intervention (PCI) or, if not available, early thrombolysis. Early B-blockade. Gradual mobilization. Do not delay arterial or central venous cannulation if cl inically indicated. An experienced operator should perform these procedures to minimize the risk of bleeding. Avoid the subclavian route. \200 \200 \200 \200 Complications of myocardial infarction \200 \200 \200 \200 Cardiopulmonary arrest. Continuing chest pain \200\224may be ischaemic or pericarditic in o rigin. Pump failure. Hypotension \200\224apart from cardiogenic shock, consider hypovolaemi a (e.g. post-diuretics) or a reaction to a thrombolytic agent. Tachyarrhythmias/bradyarrhyt hmias. Valve dysfunction \200\224predominantly mitral. Pericardial tamponade (rare). Ventri cular septal defect (unusual, often presents 2 \200\2235 days later). Complications of thro mbolytic therapy: arrhythmias, bleeding, hypotension, anaphylactoid reaction. \200 \200 \200 \200 Management of complicated infarction In addition to general measures for the uncomplicated infarction: \200 Cardiopulmonary arrest \200\224cardiopulmonary resuscitation. \200 Con tinuing ischaemic chest pain \200\224IV nitrate and heparin infusions, aspirin, clopidogrel , calcium antagonist, and B-blocker (unless contraindicated); consider urgent angiography 9 stenting or surgery. Pericarditic chest pain \200\224consider non-steroidal anti-in \202 ammatory agent. Management of heart failure. Tachyarrhythmia \200\224anti-arrhythmics, sync hronized DC cardioversion. Bradycardias \200\224chronotrope, consider temporary pacing. Val ve dysfunction \200\224heart failure management; consider surgery. Pericardial tamponade \200\224pericardial aspiration. Ventricular septal defect \200\224heart failure management, consider surgery. Management of thrombolysis complications. \200 \200 \200 \200 \200 \200 \200 ACUTE CORONARY SYNDROME (2) 391 Drug dosages Diamorphine 2.5mg IV. Repeat PRN + anti-emetic Streptokinase 1.5 million units in 100mL 0.9% saline IV over 1h rtPA (alteplase) 15mg IV bolus, then 0.75mg/kg over 30min, then 0.5mg/kg over 1h to a maximal dose of 100mg. This is then followed by heparin for 24 \200\22348 h. Tenecteplase For acute MI: IV bolus of 0.5mg/kg over 10s, followed by heparin for 24 \200\22348h. Reteplase Two IV boluses of 10U given 30min apart, followed by heparin for 24 \200\22348h. Aspirin 150mg PO od Clopidogrel 300mg PO loading dose, then 75mg PO od Atenolol 50mg PO od (increase to 100mg od if not hypotensive and HR exceeds 70bpm) or 5mg slow IV bo lus Propranolol 10 \200\22340mg PO qds (titrate to HR of 60bpm) Isosorbide dinitrate 2 \200\22340mg/h IV GTN 10 \200\223200mcg/min IV or 0.5 \200\2231mg SL Diltiazem 60mg PO tds Nifedipine 5 \200\22310mg SL or PO tds Atropine 0.3mg IV. Repeat to maximum of 2mg Lidocaine 1mg/kg slow IV bolus, then 2 \200\2234mg/min Amiodarone 5mg/kg over 20min, then infused up to 15mg/kg/d in 5% glucose via central vein. (In emergen cy, give 150 \200\223300mg in 10 \200\22320mL 5% glucose over 3min.) Key papers Task Force on management of acute myocardial infarction of the European Society of Cardiology. (2003) Management of acute myocardial infarction in patients presenting with ST segment eleva- tion. Eur Heart J 24: 28 \200\22366. Thygesen K for the Joint ESC/ACCF/AHA/WHF Task Force for the Rede \201 nition of Myocardia l Infarction. (2007) Universal de \201 nition of myocardial infarction. Circulation 116: 2 634 \200\22353. See also: Intra-aortic balloon counterpulsation, p102; Coronary revascularisation technique s, p104; ECG monitoring, p162; Echocardiography, p192; Cardiac function tests, p216; Vasodi lators, p266; Anticoagulants, p316; Thrombolytics, p320; Basic resuscitation, p338; Cardiac arrest, p340; Hypotension, p380; Tachyarrhythmias, p384; Bradyarrhythmias, p386; Acute cor onary syndrome (1), p388; Heart failure \200\224assessment, p392. 392 CHAPTER 23 Cardiovascular disorders Heart failure \200\224assessment Impaired ability of the heart to supply adequate oxygen an d nutrients to meet the demands of the body \200\231s metabolizing tissues. Major causes \200 \200 \200 \200 \200 \200 \200 \200 Myocardial infarction/ischaemia. Drugs, e.g. B-blockers, cytotoxics. Tachyarrhythmias or br adyarrhythmias. Valve dysfunction. Sepsis. Septal defect. Cardiomyopathy/myocarditis. Peric ardial tamponade. Clinical features Decreased forward \202 ow leading to poor tissue perfusion \200 \200 \200 \200 Muscle fatigue leading ultimately to hypercapnia and collapse. Confusion, agitation, drowsi ness, coma. Oliguria. Increasing metabolic acidosis, arterial hypoxaemia, and dyspnoea. Increased venous congestion secondary to right heart failure \200 \200 \200 \200 Peripheral oedema. Hepatic congestion. Splanchnic ischaemia. Raised intracranial pressure. Increased pulmonary hydrostatic pressure from left heart failure \200 \200 Pulmonary oedema, dyspnoea. Hypoxaemia. Investigations Test Diagnosis ECG Myocardial ischaemia/infarction, arrhythmias Chest X-ray With left heart failure: pulmonary oedema (interstitial perihilar ( \200\230bat \200\231s w ing \200\231) shadowing, upper lobe blood diversion, Kerley B lines, pleural effusion) 9 ca rdiomegaly Low cardiac output and stroke volume, low mixed venous oxygen saturation (<60%), raised PAWP (with left heart failure), raised RAP (with right heart failure). V waves with mitral or tricuspid regurgitation Flow monitoring Blood tests Low SaO2, variable PaCO2, base de \201 cit >2 mmol/L, hyperlactataemia, low venous O2, (mi xed or central venous), raised cardiac enzymes, troponin, BNP, thyroid function (if indicat ed) Echocardiogram Poor myocardial contractility, ventricular akinesia, hypokinesia or dyskinesia, pericardial effusion, valve stenosis or incompetence Notes Peripheral oedema implies total body salt and water retention, but not necessarily in travascular \202 uid overload. HEART FAILURE \200\224ASSESSMENT 393 See also: IPPV \200\224assessment of weaning, p60; Pulse oximetry, p144; Blood gas analysis , p154; Respiratory imaging, p158; ECG monitoring, p162; Blood pressure monitoring, p164; C entral venous cateter \200\224 use, p170; Cardiac output \200\224central thermodilution, p1 78; Cardiac output \200\224peripheral thermodi- lution, p180; Cardiac output \200\224indica tor dilution, p182; Cardiac output \200\224Doppler ultrasound, p184; Cardiac output \200 \224pulse contour analysis, p186; Cardiac output \200\224other techniques, p188; Echocardio graphy, p192; Tissue perfusion monitoring, p194; Cardiac function tests, p216; Dyspnoea, p2 46; Respiratory failure, p350; Hypotension, p380; Tachyarrhythmias, p384; Bradyarrhythmias, p386; Acute coronary syndrome (1), p388; Acute coronary syndrome (2), p390; Heart failure \200\224 management, p392. 394 CHAPTER 23 Cardiovascular disorders Heart failure \200\224management Basic measures 1. Determine likely cause and treat as appr opriate, e.g. anti-arrhythmic. 2. Oxygen \200\224to maintain SaO2 \211 98%. 3. GTN spray S L, then commence IV nitrate infusion titrated rapidly until good clinical effect. Beware hy potension which, at low dosage, is sug- gestive of left ventricular under \201 lling, e.g. hypovolaemia, tamponade, mitral stenosis, pulmonary embolus. 4. If patient agitated or in pain, give diamorphine IV. 5. Consider early CPAP, BiPAP, and/ or IPPV to reduce work of breathing and provide good oxygenation. Cardiac output will often improve. Do not delay until the patient is in extremis. 6. Furosemide is rarely needed as \201 rst-line therapy unless intravascular \202 uid o verload is causative. Initial symptomatic relief is provided by its prompt vasodilating act ion; however, subsequent diuresis may result in marked hypovolaemia leading to compensatory vasoconstriction, increased cardiac work, and worsening myocardial function. Diuretics may be indicated for acute-on-chronic failure, especially if the patient is on long-term diure tic therapy, but should not be used if hypovolaemic. If furosemide is required, start at lo w doses, then reassess. Directed management 1. Adequate monitoring (9 cardiac output) and investigation (echocardi- ography). 2. Avoid hypovolaemia (e.g. diuretics given). Fluid challenge if necessary. 3. If vasoconst riction persists (high BP, low cardiac output), titrate nitrate infusion to optimize stroke volume. Allow BP to fall if well-perfused. If hypovolaemia is suspected (i.e. stroke volum e falls), give \202 uid challeng- es to re-optimize stroke volume. Within 24 hours of nit rate infusion, commence ACE inhibition, initially at low dose but rapidly increased to appr opriate long-term doses. 4. Inotropes are needed if tissue hypoperfusion, hypotension, or vaso- constriction persist s despite optimal \202 uid loading and nitrate dosing. Consider epinephrine, dobutamine, or milrinone. Epinephrine may sometimes cause excessive constriction; dobutamine, and milri none may excessively vasodilate. Levosimendan increases cardiac output through improving co ntractile ef \201 ciency. 5. Intra-aortic balloon counterpulsation augments cardiac output, reduces cardiac work, and improves coronary artery perfusion. 6. Angioplasty or surgical revascularisation is bene \201 cial if performed early after my ocardial infarct. Surgery may also be necessary for mechanical defects, e.g. acute mitral r egurgitation. Treatment endpoints 1. BP and cardiac output adequate to maintain organ perfusion (e.g. no oliguria, confusion, dyspnoea nor metabolic acidosis). Avoid treatment of blood pressure if organs are perfused. 2. Mixed (or central) venous oxygen saturation \211 60%. Excessive inotropes should be avoided as myocardial O2 demand is increased. 3. Symptomatic relief. HEART FAILURE \200\224MANAGEMENT 395 Drug dosages GTN 2 \200\22340mg/h IV or 0.4 \200\2230.8mg by SL spray Isosorbide dinitrate 2 \200\22340mg/h IV Nesiritide 2mcg/kg bolus followed by infusion of 0.01 \200\2230.03mcg/ kg/min Sodium nitroprusside 20 \200\223400mcg/min IV Captopril 6.25mg PO test dose increasing to 25mg tds Enalapril 2.5mg PO test dose increasing to 40mg od Lisinopril 2.5mg PO test dose increasing to 40mg od Epinephrine Infusion starting from 0.05mcg/kg/min Dobutamine 2.5 \200\22325mcg/kg/min IV Dopamine 2.5 \200\22325mcg/kg/min IV Milrinone Loading dose of 50mcg/kg IV over 10min, followed by infusion from 0.375 \200\2230.75mcg/kg/ min Enoximone Loading dose of 0.5 \200\2231mg/kg IV over 10min, followed by infusion from 5 \200\22320mcg /kg/min Levosimendan 12 \200\22324 mcg/kg over 10min, followed by 0.1mcg/kg/ min for 24h Diamorphine 2.5mg IV. Repeat every 5min as necessary. Furosemide 10 \200\22320mg IV bolus. Repeat or increase as necessary. Key papers Cotter G, Metzkor E, Kaluski E, et al. (1998) Randomized trial of high-dose isos orbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorb ide dinitrate in severe pulmonary oedema. Lancet 351: 389 \200\22393. Cuffe MS, Califf RM, Adams KF, et al. (2000) Rationale and design of the OPTIME CHF trial: out- comes of a prospective trial of intravenous milrinone for exacerbations of chronic hea rt failure. Am Heart J 139: 15 \200\22322. Follath F, Cleland JG, Just H, et al. (2002) Ef \201 cacy and safety of intravenous levosi mendan compared with dobutamine in severe low-output heart failure (the LIDO study): a rand omized double-blind trial. Lancet 360: 196 \200\223202. Nieminen MS, for the ESC Committe for Practice Guideline (CPG). (2005) Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Ac ute Heart Failure of the European Society of Cardiology. Eur Heart J 26: 384 \200\223416. Peter JV, Moran JL, Phillips-Hughes J, et al. (2006) Effect of non-invasive positive pressu re ventila- tion (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet 367: 1155 \200\22363. See also: Oxygen therapy, p38; Endotracheal intubation, p42; Ventilatory support \200\224in dications, p44; Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68; Continuous positive This page intentionally left blank 397 Chapter 24 Renal disorders Oliguria 398 Acute renal failure \200\224diagnosis 400 Acute renal failure \200\224manageme nt 402 398 CHAPTER 24 Renal disorders Oliguria De \201 ned as a urine output <0.5mL/kg/h and caused by: \200 Post-renal \200\224urinary tract obstruction, e.g. blocked catheter, ureteric trauma, prost atism, raised intra-abdominal pressure, blood clot, bladder tumor. Renal \200\224establishe d acute renal failure, acute tubular necrosis (rare), glomerulonephritis. Pre-renal \200 \224hypovolaemia, low cardiac output, hypotension, inadequate renal blood \202 ow. Obstruction and pre-renal causes of oliguria must be excluded before resorting to diuretics . Urinary tract obstruction A full bladder should be excluded by palpation. Ensure a patent c atheter is present. If obstruction is due to blood clot, the bladder should be irri- gated. If obstruction is suspected higher in the renal tract, an ultrasound scan is required for diagnosis and possible intervention (e.g. nephrosto- mies). Raised intra-abdominal pressure may cause oliguria by impeding renal venous drainage (particularly if >20mmHg). Relief of the high pressure often promotes a diuresis. Hypovolaemia Once renal tract obstruction is excluded, it is mandatory to correct hypo- vol aemia by \202 uid challenge. Oliguria in hypovolaemic patients may be physiological or ma y be due to a reduced renal blood \202 ow. Inadequate renal blood \202 ow and/or pressure If cardiac output remains low despite corr ecting hypovolaemia, vasodi- lators and/or inotropes may be needed. If BP remains low after cardiac output is improved, vasopressors may be needed to achieve a mean BP of \211 60mmH g. In the elderly and those with pre-existing hypertension, a higher mean BP may be necessa ry to maintain urine output. Persistent oliguria Attempts to increase urine output with diuretics may follow the above m easures if oliguria persists. Furosemide is given at a dose of 5 \200\22310mg IV with highe r increments at 30min intervals to a maximum of 250mg. High doses or a low-dose infusion (1 \200\2235mg/h IV) may be needed if the patient has previously received diuretic.s. Mannito l (20g IV) may be considered though failure to promote diuresis may increase oedema formati on. Failure to re-establish urine output may require renal support in the form of dial- ysi s or haemo \201 ltration. There is no point in continuing diuretic therapy if it is not ef fective; loop diuretics in particular may be nephrotoxic. Indications for renal support inc lude \202 uid overload, hyperkalaemia, metabolic acidosis, creation of space for nutritio n or drugs, persistent renal failure with rising urea and creatinine, and symptomatic uraem ia. OLIGURIA 399 Biochemical assessment (not applicable if furosemide has been given previously) Pre-renal cause Renal cause Urine osmolality (mOsm/kg) >500 <400 >40 Urine Na (mmol/L) <20 <20 Urine : plasma creatinine >40 Fractional Na excretion* <1 >2 : urine plasmaNa \227 100 : urine plasma creatinine See also: Urea and creatinine, p210; Electrolytes (Na+, K+, Cl \200\223, HCO3 \200\223), p 212; Urinalysis, p232; Basic resus- citation, p338; Fluid challenge, p342; Acute renal fail ure \200\224diagnosis, p400; Raised intra-abdominal pressure, p614; Post-operative critical care, p620. 400 CHAPTER 24 Renal disorders Acute renal failure \200\224diagnosis Renal failure is de \201 ned as renal function inade quate to clear the waste products of metabolism despite absence or correction of haemodynam ic or mechanical causes. Renal failure is suggested by: \200 \200 \200 \200 \200 Uraemic symptoms (drowsiness, nausea, hiccough, twitching). Raised plasma creatinine (>200 mol/L). Hyperkalaemia. Hyponatraemia. Metabolic acidosis. Persistent oliguria may be a feature of acute renal failure, but non-oliguric renal failure is common; 2 \200\2233L of poor quality urine per day may occur despite inadequate glomeru lar \201 ltration. The prognosis is better if urine output is maintained. Clinical featur es may suggest the cause of renal failure and dictate further investigation. Acute tubular necrosis may occur following rapid loss of perfusion, e.g. major hemorrhage. However, it is a misnomer in renal failure due to sepsis, pancreatitis, etc., as minimal cell death is se en. Anemia suggests chronic renal failure. Post-operative renal failure Risk factors include hypovolaemia, haemodynamic instability (p articularly hypotension), major abdominal surgery in those >50 years, major surgery in jaun diced patients, biliary and other sepsis. Surgical procedures (particu- larly gynecological ) may be complicated by damage to the lower urinary tract with an obstructive nephropathy. Abdominal aortic aneurysm surgery may be associated with renal arterial disruption and shou ld be investigated urgently with renography and possible arteriography or re-exploration. Other causes \200 Nephrotoxins \200\224may cause renal failure via acute tubular necrosis, interstitial nephr itis, or renal tubular obstruction. All potential nephrotoxins should be withdrawn. Rhabdom yolysis \200\224suggested by myoglobinuria and raised CPK in patients who have suffered a c rush injury, coma, or seizures. Glomerular disease \200\224red cell casts, haematuria, prot einuria, and systemic features (e.g. hypertension, purpura, arthralgia, vasculitis) are all suggestive of glomerular disease. Renal biopsy or speci \201 c blood tests (e.g. Goodpast ure \200\231s syndrome, vasculitis) are required to con \201 rm diagnosis and appropriate treatment. Haemolytic uraemic syndrome \200\224suggested by haemolysis, uraemia, thrombocyt opaenia, and neurological abnormalities. Crystal nephropathy \200\224suggested by the prese nce of crystals in the urinary sediment. Microscopic examination of the crystals con \201 rms the diagnosis (e.g. urate, oxalate). Release of purines and urate are responsible for a cute renal failure in the tumor lysis syndrome. Renovascular disorders \200\224loss of vasc ular supply may be diagnosed by renography. Complete loss of arterial supply may occur in a bdominal trauma or aortic disease (particularly dissection). More commonly, the arterial su pply is partially compromised (e.g. renal artery stenosis) and blood \202 ow is further r educed by haemodynamic instability or locally via drug therapy (e.g. NSAIDs, ACE inhibitors ). Renal vein obstruction may be due to thrombosis or external compression (e.g. raised int ra-abdominal pressure). ACUTE RENAL FAILURE \200\224DIAGNOSIS 401 Nephrotoxins The following are some common nephrotoxins: Allopurinol Aminoglycosides Amphotericin Cephalosporins Dextran 40 Furosemide Heavy metals Herbal medicines Narcotics NSAIDs Organic solvents Paraquat Penicillins Pentamidine Phenytoin Radiographic contrast Sulphonamides Tetracyclines Thiazides Vancomycin Key papers Thurau K, Boylan JW. (1976) Acute renal success. The unexpected logic of oliguri a in acute renal failure. Am J Med 61: 308 \200\22315. Wan L, Bagshaw SM, Langenberg C, et al. (2008) Pathophysiology of septic acute kidney injur y: what do we really know? Crit Care Med 36(4 Suppl): S198 \200\223203. See also: Blood pressure monitoring, p164; Urea and creatinine, p210; Electrolytes (Na+, K+ , Cl \200\223, HCO3 p212; Full blood count, p220; Urinalysis, p232; Hypotension, p380; Hear t failure \200\224assessment, p392; Oliguria, p398; Acute renal failure \200\224management, p402; Intra-abdominal bowel perforation and obstruction, p418; Abdominal sepsis, p422; Pan creatitis, p424; Jaundice, p428; Acute liver failure, p430; Vasculitis, p574; Rhabdomyolysi s, p612; Raised intra-abdominal pressure, p614; Post-operative critical care, p620. \200\223), 402 CHAPTER 24 Renal disorders Acute renal failure \200\224management \200 \200 \200 Identify and correct reversible causes. Attend to \202 uid management and nutritional sup port carefully. Early use of renal replacement techniques allow normal \202 uid and nutri tional intake and may improve outcome. Mortality in the setting of acute renal failure in the critically ill is high (50 \200\2236 0%). In surviving patients, permanent renal failure is rare with recovery usually seen within 1 \200\2236 weeks. Urinary tract obstruction \200 Decompress lower urinary tract obstruction with a urinary catheter (suprapubic if there is urethral disruption). Decompress ureteric obstruction by nephrostomy or stent. Massive diuresis is common after urinary tract decompression so ensure an adequate circulat ing volume to prevent secondary pre-renal failure. Haemodynamic management \200 \200 The circulating volume must be corrected \201 rst. Prompt restoration of circulating volu me, and any necessary inotrope or vasopressor support may reverse pre-renal failure. Diuret ics (furosemide, mannitol) may establish a diuresis if oliguria persists after pre-renal fa ctors have been corrected. Urgent treatment of hyperkalaemia \200 \200 \200 10 \200\22320mL 10% calcium chloride by slow IV injection. 100mL 8.4% sodium bicarbonate IV (centrally). Glucose (50g) and insulin (10 \200\22320IU) IV with careful blood glucose mon itoring. Urgent renal replacement therapy. Metabolic management \200 Hypocalcaemia is best treated with renal replacement and calcium supplementation. Hyponatra emia is usually due to water excess although salt-losing nephropathies may require sodium c hloride supplements. Hyperphosphataemia may be treated with renal replacement or aluminum h ydroxide PO. Metabolic acidosis (not due to tissue hypoperfusion) may be corrected with dia lysis, \201 ltration, or a 1.26% sodium bicarbonate infusion. Renal replacement therapy Continuous haemo \201 ltration forms the mainstay of replacement therapy in critically ill patients who may not tolerate haemodialysis. Nephrotoxins and crystal nephropathies Nephrotoxic agents should be withheld if possible. D rug dosage should be modi \201 ed according to GFR. In some cases, urinary excretion of ne phro- toxins and crystals may be encouraged by urinary alkalinisation. Glomerular disease Immunosuppressive therapy may be useful. Dialysis is often required for the more severe forms despite steroid responsiveness. ACUTE RENAL FAILURE \200\224MANAGEMENT 403 General indications for dialysis or haemo(dia) \201 ltration \200 \200 \200 \200 \200 \200 \200 \200 Fluid excess (e.g. pulmonary oedema). Hyperkalaemia (>6.0mmol/L). Metabolic acidosis (pH<7. 2) due to renal failure. Clearance of dialysable nephrotoxins and other drugs. Creatinine r ising >100 mol/L/d. Creatinine >300 \200\223600 mol/L. Urea rising >16 \200\22320mmol/L/d . To create space for nutrition or drugs. See also: Haemo(dia) \201 ltration (1), p108; Haemo(dia) \201 ltration (2), p110; Periton eal dialysis, p112; Plasma exchange, p114; Urea and creatinine, p210; Electrolytes (Na+, K+ , Cl \200\223, HCO3 p242; Colloids, p246; Diuretics, p280; Oliguria, p398; Acute renal fail ure \200\224diagnosis, p400; Electrolyte management, p482; Hyperkalaemia, p488; Metabolic a cidosis, p502. \200\223), p212; Crystalloids, This page intentionally left blank 405 Chapter 25 Gastrointestinal disorders Vomiting/gastric stasis 406 Diarrhea 408 Failure to open bowels 410 Upper gastrointestinal hemorrhage 412 Bleeding varices 414 Oesophageal perforation 416 Intra-abdominal bowel perfo ration and obstruction 418 Lower intestinal bleeding and colitis 420 Abdominal sepsis 422 P ancreatitis 424 406 CHAPTER 25 Gastrointestinal disorders Vomiting/gastric stasis While vomiting per se is relatively rare in the ICU patient, large volume gastric aspirates are commonplace and probably represent the major reason for failur e of enteral nutrition. General principles \200 \200 Seek an underlying cause. Ensure volaemic and total body \202 uid status is adequate, esp ecially as aspirates can exceed several litres/day. Monitor and correct electrolyte abnorma lities, e.g. metabolic alkalosis, hypokalaemia. Oesophageal rupture (Boerhaave \200\231s sy ndrome) should be considered if vomiting forceful. Ileus Ileus affects the stomach more frequently than the rest of the GI tract. Abdominal su rgery, drugs (particularly opiates), gut dysfunction as a component of multi-organ dysfunct ion, hypoperfusion, and prolonged starvation may all contribute to gastric ileus. Early and continued use of the bowel for feeding appears to maintain forward propulsive action. Mana gement consists of treating the cause where possible. Consider the use of motility stimulan ts such as metoclopramide or erythromycin, and in resistant cases, bypassing the stomach wi th a nasoduodenal/nasojejunal tube or a jejunostomy. Caution should be exercised with effor ts to estab- lish enteral feeding if the patient has increasing abdominal distension and/ o r pain, or an explained and increasing metabolic acidosis. Bowel rest and/ or parenteral fe eding may be indicated if symptoms fail to settle. Upper bowel obstruction Relatively unusual; apart from primary surgical causes such as neop lasm or adhesions, the predominant cause in the ICU is gastric outlet obstruction. This may be related to longstanding peptic ulcer disease or occur in the short term from pyloric an d/or duodenal swelling consequent to gastritis or duodenitis. This can be diagnosed endosco pically and treated by bowel rest plus an H2 antagonist, proton pump inhibitor, or sucralfa te. Gastric irritation Drugs or chemicals, either accidental or adverse reaction (e.g. corticos te- roids, aspirin), intentional (e.g. alcohol, bleach) or therapeutic (e.g. ipeca- cuanha syrup) may induce vomiting. Treatment, where appropriate, may comprise: (i) removal of the cause, (ii) dilution with copious amounts of \202 uid, (iii) neutralization with alkali a nd/or H2 antagonist or proton pump inhibitor, and (iv) administration of an anti-emetic, e. g. metoclopramide. Neurological Stimulation of the emetic center may follow any neurological event (e.g. traum a, CVA), drug therapy (e.g. chemotherapy), pain and metabolic dis- turbances. Management is by treating the cause where possible and by judicious use of anti-emetics, initially metoc lopramide or prochlorpera- zine. Consider ondansetron if these are unsuccessful. VOMITING/GASTRIC STASIS 407 See also: Upper gastrointestinal endoscopy, p120; Enteral feeding and drainage tubes, p122; Enteral nutri- tion, p128; Electrolytes (Na+, K+, Cl \200\223, HCO3 Upper gastrointestinal hemorrhage, p412; Bleeding varices, p414; Oesophageal perforation, p416; Intra-abdominal b owel perforation and obstruction, p418; Intracranial hemorrhage, p448; Subarachnoid hemorrh age, p450; Stroke, p452; Raised intracranial pressure, p454; Hypokalaemia, p490; Metabolic alkalosis, p504; Diabetic ketoacidosis, p510; Head injury (1), p586; Head injury (2), p588; Pain, p618; Effects of chemo- and radiotherapy, p626. \200\223), p212; Anti-emetics, p292; Gut motility agents, p294; 408 CHAPTER 25 Gastrointestinal disorders Diarrhea The de \201 nition of diarrhea in the ICU patient is problematic as the amount of stool passed daily is dif \201 cult to measure. Frequency and con- sistency may also vary signi \201 cantly. Loose/watery and frequent ( \211 4x per day) stool will often require investigation and/or treatment. Common ICU causes \200 Infection \200\224Clostridium (C.) dif \201 cile, gastroenteritis (e.g. Salmonella, Shigel la), rarer tropical causes (e.g. cholera, dysentry, giardiasis). Drugs, e.g. antibiotics, l axatives. Gastrointestinal \200\224feed (e.g. lactose intolerance), coeliac disease, other malabsorption syndromes, in \202 ammatory bowel disease, diverticulitis, pelvic abscess, b owel obstruction with over \202 ow. \200 Enteral feed is often implicated but rarely causative. For bloody diarrhea consider infection, ischaemic or in \202 ammatory bowel disease. Diagnosis \200 Rectal examination to exclude impaction with over \202 ow. Consider sigmoidoscopy if colit is or C. dif \201 cile suspected (in the latter, a pseudomembrane is seen). Stool sent to laboratory for M, C & S, C. dif \201 cile toxin. Fat estimation (malabsorption) is rarely necessary in the ICU patient. If ischaemic or in \202 ammatory bowel disease suspected, pe rform a CT or supine abdominal X-ray and inspect for dilated loops of bowel (NB. toxic mega colon), thickened walls (increased separation between loops), and \200\230thumbprinting \200\231 (suggestive of mucosal oedema). Fluid levels seen on erect or lateral abdominal X- ray may be seen in diarrhea or paralytic ileus and do not necessarily indicate obstruction. Diarrhea is often, but not always, bloody. If abscess suspected, perform ultrasonography o r CT scan. \200 \200 Management \200 Treat cause where possible, e.g. for C. dif \201 cile, metronidazole plus colestyramine (b inds the toxin). Anecdotal success has been reported with immunoglobulin therapy for C. dif \201 cile colitis. Consider temporary (12 \200\22324h) cessation of enteral feed if very severe. Consider changing feed if appropriate, e.g. coeliac disease, lactose intolerance. C onsider stopping antibiotics. Give anti-diarrhoeal if infection excluded. Careful attention to \202 uid and electrolyte balance (in particular Na+, K+, Mg2+). Request surgical opin ion for possible colectomy if infarcted or in \202 amed bowel, toxic dilatation, or absces s suspected. \200 \200 diarrhea 409 See also: Enteral nutrition, p128; Electrolytes (Na+, K+, Cl \200\223, HCO3 serology, and a ssays, p226; Antidiarrhoeals, p296; Lower intestinal bleeding and colitis, p420. \200\223), p212; Bacteriology, p224; Virology, 410 CHAPTER 25 Gastrointestinal disorders Failure to open bowels Common ICU causes \200 \200 \200 Prolonged ileus/decreased gut motility (e.g. opiates, post-surgery). Lack of enteral nutrit ion. Bowel obstruction \200\224this is a relatively uncommon secondary event and is mainly seen post-operatively, either after a curative procedure or with development of adhesions. Management \200 Clinically exclude obstruction and con \201 rm presence of stool per rectum. Ensure adequa te hydration. Anti-constipation therapy may be given, usually starting with laxatives (e.g. lactulose or, for more urgent response, magnesium sulfate), then proceeding to glycerin su ppositories, and \201 nally, enemata if gentler measures prove unsuccessful. Consider red ucing/stopping dose of opiate if possible. For colonic pseudo-obstruction, consider 2mg IV neostigmine. \200 \200 FAILURE TO OPEN BOWELS 411 Key paper Robert J. Ponec RJ, Saunders MD, et al. (1999) Neostigmine for the treatment of a cute colonic pseudo-obstruction. N Engl J Med 341: 137 \200\22341. See also: Anti-constipation agents, p298; Intra-abdominal bowel perforation and obstruction , p418; Abdominal sepsis, p422; Pancreatitis, p424. 412 CHAPTER 25 Gastrointestinal disorders Upper gastrointestinal hemorrhage Causes \200 \200 \200 \200 \200 Peptic ulceration. Oesophagitis/gastritis/duodenitis. Varices. Mallory \200\223Weiss lower oesophageal tear. Neoplasms. Pathophysiology Peptic ulceration is related to protective barrier loss leading to acid or biliary damage of the underlying mucosa and submucosa. Barrier loss occurs secondary to cri tical illness, alcohol, and drugs, e.g. non-steroidals, poisons, including corrosives. Dire ct damage, especially at the lower esophagus, may occur from feeding tubes. Mucosal damage ( \200\230stress ulcers \200\231) may also occur as a consequence of tissue hypoperfusion. Gastric hypersecretion is uncommon in critically ill patients; indeed, gastric acid content and secretion are often reduced. Prophylaxis \200 \200 Small-bore feeding tubes. Nasogastric enteral nutrition (even nasojejunal and parenteral fe eding have also been shown to reduce the incidence of stress ulcer bleeding). Adequate tiss ue perfusion ( \202 ow and pressure). Prophylactic drug therapy (proton pump inhibitor, H2 antagonist) decreases the incidence of stress ulceration though this is largely based on h istoric data when gut hypoperfusion was more prevalent. Patients at highest risk for stress ulcers are those requiring prolonged mechanical ventilation or with a concurrent coagulopa thy. \200 Treatment of major hemorrhage \200 Fluid resuscitation with colloid and blood, with blood products as appropriate to correct a ny coagulopathy. Maintain Hb >7 \200\22310g/dL and have adequate crossmatched blood availab le should further large hemorrhages occur. If possible, discontinue any ongoing anticoagula tion, e.g. heparin. Urgent diagnostic \201 breoptic endoscopy. Local injection of epineph rine or a sclerosant into (or thermal sealing of) a bleeding peptic ulcer base may halt fur ther bleeding. Banding or sclerosant injection may arrest bleeding varices. If oesophageal varices are known or highly suspected, consider vasopressin or terlipressin 9 a Sengstaken- type tube for severe hemorrhage, either as a bridge to endoscopy or if banding/injection is unsuccessful. Remember that sources of bleeding other than varices may be present, e.g. pe ptic ulcer. For peptic ulceration and generalized in \202 ammation, commence H2 antagonist or proton pump inhibitor. Give IV to ensure effect. Enteral antacid may also be bene \201 cial. For continued bleeding, contact interventional radiologist with view to angiographic embolisation. Surgery is now rarely necessary, but should be considered if bleeding contin ues, e.g. >6 \200\22310 unit transfusion need and embolisation is not available or fails. I nform surgeon of any patient with major bleeding. \200 UPPER GASTROINTESTINAL hemorrhage 413 See also: Sengstaken-type tube, p118; Full blood count, p220; Coagulation monitoring, p222; Colloids, p246; Blood transfusion, p248; Blood products, p250; H2 blockers and proton pump inhibitors, p286; Sucralfate, p288; Antacids, p290; Basic resuscitation, p338; Bleeding va rices, p414. 414 CHAPTER 25 Gastrointestinal disorders Bleeding varices Varices develop following a prolonged period of portal hypertension, usual ly related to liver cirrhosis. Approximately one third will bleed. They are commonly found in the lower esophagus, but occasionally in the stomach or duodenum. Torrential hemorrhage may occur. Approximately 50% of patients die within six weeks of presentation of their \201 rst bleed; each subsequent bleed carries a 30% mortality. Management 1. If airway and/or breathing are compromised, perform endotracheal intubation a nd institute mechanical ventilation. This facilitates Sengstaken- type tube placement and e ndoscopy though may be associated with severe hypotension secondary to covert hypovolaemia. If possible, en- sure adequate intravascular \201 lling before intubation. 2. Fluid resuscitation with colloid and blood with blood products as ap- propriate to corre ct any coagulopathy. Ensure good venous access (at least two 14G cannulae). Group-speci \201 c or O-negative blood may be needed for emergency use. Maintain Hb >7 \200\22310g/dL a nd have at least four units of crossmatched blood available for urgent transfusion. There i s a theoretical risk that over-transfusion may precipitate further bleeding by raising port al venous pressure. Cardiac output monitoring should be considered if the patient remains h aemodynamically unstable or there is a history of heart disease. 3. If bleeding is torrential, insert a Sengstaken-type tube and commence administration of IV vasopressin/terlipressin (q.v.). 4. Gentle placement of a large-bore nasogastric tube is a reasonably safe procedure that fa cilitates drainage of blood, lessens the risk of aspira- tion, and can be used to assess co ntinuing blood loss. 5. Perform urgent \201 breoptic endoscopy to exclude other sources of bleeding. This also allows variceal banding or local injection of scleros- ing agent. Bleeding is arrested in approximately 90% of cases. Endoscopy may be impossible if bleeding is too severe, and may have to be delayed for 6 \200\22324h until a period of tamponade by the Sengstaken-type tub e 9 vasopressin has enabled some control of the bleeding. 6. Either vasopressin, terlipressin, or octreotide can be administered for severe bleeding or prophylaxis against fresh bleeding. Vasopressin con- trols bleeding in approximately 60% of cases and its ef \201 cacy and safety appears to be enhanced by concurrent GTN. The si de effect pro \201 le of terlipressin is lower as it does not appear to precipitate as muc h me- senteric, cardiac, or digital ischaemia. Octreotide is a somatostatin ana- logue, but longer-acting than its parent compound; like somatostatin, it is probably as effective as vasopressin but without the side effects. 7. If bleeding continues after prolonged balloon tamponade (2 \200\2233 days) and repeated endoscopy, consider transjugular intrahepatic por tosys- temic stented shunt (TIPSS). This can be performed quickly and carries a relatively low mortality compared to surgery although the risk of encephalopathy is increased. 8. The traditional alternative to TIPSS is oesophageal transection (now performed with a st aple gun) with or without devascularisation. Mortality in the acute situation is of the ord er of 30%. BLEEDING VARICES 415 Drug dosages Octreotide 50mcg bolus, then 50mcg/h infusion Vasopressin 20 units over 20min, then 0.4 units/min infusion Also give glyceryl trinitrate 2 \200\22320mg/h to counteract myocardial and mesenteric isch aemia. Terlipressin 2 mg IV, followed by 1 \200\2232mg IV 4 \200\2236 hourly until bleeding controlled for up t o 72h