Q: What is the usual cut off point in size to consider immediate drainage for renal abscess and perirenal abscess respectively? 


Answer: 5 cm and 3 cm respectively

Though both starts as tissue necrosis due to infection, renal and perinephric abscess are two different processes, at least in terms of location, which may make managements little different. A renal abscess is a walled-off cavity inside the kidney, and the perinephric abscess is relatively a liquefied substance lying between the renal capsule and Gerota’s fascia. 

Renal abscesses can be managed conservatively until the size is about 5 cm, but perinephric abscesses should be drained relatively early at around 3 cm. This is just a rule of thumb, as smaller abscesses may require percutaneous or surgical interventions if antibiotics remain ineffective.

This leeway is due to the reason that renal abscess usually responds well to a proper antibiotic regimen, as well as drainage can be relatively difficult. Also, as perinephric abscesses do not communicate with the collecting system, there is no other way to obtain culture/microorganism except direct intervention to tailor proper antibiotics.


References:

1.  Lee SH, Jung HJ, Mah SY, Chung BH. Renal abscesses measuring 5 cm or less: outcome of medical treatment without therapeutic drainage. Yonsei Med J 2010; 51:569.

2. Dalla Palma L, Pozzi-Mucelli F, Ene V. Medical treatment of renal and perirenal abscesses: CT evaluation. Clin Radiol 1999; 54:792.

3. Coelho RF, Schneider-Monteiro ED, Mesquita JL, et al. Renal and perinephric abscesses: analysis of 65 consecutive cases. World J Surg 2007; 31:431.

4. Meng MV, Mario LA, McAninch JW. Current treatment and outcomes of perinephric abscesses. J Urol 2002; 168:1337.

Q: Gastric-arterial pCO2 gradient continues to remain a controversial parameter to measure in septic shock. Given, if it is use in clinical practice, what is the cutoff level to designate patient at high risk of dying from septic shock? 

 Answer: 15 mm Hg

Gastric-arterial pCO2 gradient has been suggested as a prognostic marker in patients with septic shock, as it may measure the end organ ischemia. Gastric PCO2 is measured by gastric tonometry, which indirectly measures the perfusion to the gut. Theoretically,  trending gastric to arterial PCO2 gap should reflect the end organ ischemia, but evidence based literature failed to show its clinical relevance. 

On similar line, attempts have been made to calculate and trend  gastric PCO2-(End-tidal) PCO2 gap, but so far there is no real success.

 
Reference: 

1. Gutierrez G, Palizas F, Doglio G, et al. Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients. Lancet 1992; 339:195. 

2. Uusaro A, Russell JA, Walley KR, Takala J - Gastric-arterial PCO2 gradient does not reflect systemic and splanchnic hemodynamics or oxygen transport after cardiac surgery - Shock. 2000 Jul;14(1):13-7. 

Q: What is the most common causative organism associated with non-central line associated jugular vein suppurative thrombophlebitis?


Answer: Fusobacterium necrophorum

Jugular vein suppurative thrombophlebitis, commonly known as Lemierre's syndrome is usually caused by either central line or extension of oropharyngeal infection. Causative organisms are different respectively.

Clinical significance: Initial empiric treatment for Fusobacterium necrophorum should include a beta-lactamase resistant beta-lactam antibiotic like ampicillin-sulbactam, piperacillin-tazobactam, ticarcillin-clavulanate or a carbapenem. Jugular vein suppurative thrombophlebitis secondary to central line catheter should include vancomycin in the initial empiric therapy to cover skin flora.

Later antibiotics can be tailored and narrowed according to culture and sensitivity.



Reference:

1. Chirinos JA, Lichtstein DM, Garcia J, Tamariz LJ. The evolution of Lemierre syndrome: report of 2 cases and review of the literature. Medicine (Baltimore) 2002; 81:458. 

2. Hagelskjaer Kristensen L, Prag J. Lemierre's syndrome and other disseminated Fusobacterium necrophorum infections in Denmark: a prospective epidemiological and clinical survey. Eur J Clin Microbiol Infect Dis 2008; 27:779.

Q: What is NCDR CathPCI risk score?

Answer:  National Cardiovascular Data Registry (NCDR) for percutaneous coronary intervention (PCI) is a model to predict initial risk in patients with coronary artery disease undergoing PCI. It  was developed from little less than 200,000 patients over 3 years across United States. It took into account of 21 variables including age, CHF status, renal insufficiency, PVD, respiratory status, and level of EKG status (STMI or NSTMI), and others.

It is a very strong data (C-Index). Patients were equally divided into two arms - patients with acute coronary syndrome and stable patients. Overall in-hospital mortality following PCI was 0.65 percent in elective cases and 4.81 percent in ST-elevation MI patients.


Reference:

1. Peterson ED, Dai D, DeLong ER, et al. Contemporary mortality risk prediction for percutaneous coronary intervention: results from 588,398 procedures in the National Cardiovascular Data Registry. J Am Coll Cardiol 2010; 55:1923.

Q: What is the caveat of measuring fibrinogen level in patients with liver disease? 


Answer:  Liver disease is mostly marked by (acquired) dysfibrinogenemia, not low fibrinogen level. This results in normal fibrinogen levels when measured by immunologic methods. Dysfibrinogenemia can be establish by demonstrating prolong thrombin and reptilase times.

Clinically, this is important as clinicians may get deceived by normal fibrinogen level but patient may continue to bleed due to dysfibrinogenemia.


References:

1.  Francis JL, Armstrong DJ. Acquired dysfibrinogenaemia in liver disease. J Clin Pathol 1982; 35:667. 

2. Regañón E, Vila V, Aznar J, et al. Study of the formation of fibrin clot in cirrhotic patients. An approach to study of acquired dysfibrinogenemia. Thromb Res 1987; 46:705. 

3. Mammen EF. Coagulopathies of liver disease. Clin Lab Med 1994; 14:769.

Q: Vasospasm usually occurs after day 3 in subarachnoid haemorrhage (SAH). What is the main risk factor of vasospasm happening within first 3 days of SAH?

 A) Severe SAH 
B) Female gender
C) Young  age 
D) Smoking
E) Prior SAH


Answer: E

It is true that all of the above increase the risk of vasospasm in SAH, but it usually occurs from day 3 to day 21, peaks around day 7 and risk subsequently decreases after day 12-14. But with patients who have prior SAH (may have gone unnoticed), there is a high risk of vasospasm happening before day 3.


Further reading:

1. E. Sander Connolly, Alejandro A. Rabinstein, J. Ricardo Carhuapoma, Colin P. Derdeyn, Jacques Dion, Randall T. Higashida, Brian L. Hoh, Catherine J. Kirkness, Andrew M. Naidech, Christopher S. Ogilvy, Aman B. Patel, B. Gregory Thompson, Paul Vespa - Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association - Stroke. 2012;43:1711-1737,  Originally published May 25, 2012 - http://stroke.ahajournals.org/content/43/6/1711

Q: All of  the following are risk factors of exacerbation of Tricuspid Regurgitation (TR) after insertion of  endocardial pacemaker/defibrillator?

A) Impingement of leads on a tricuspid valve leaflet
B) Tethering of  leads to the leaflet of tricuspid valves 
C) Perforation of  leads via leaflet of tricuspid valves
D) Entanglement of leads with subvalvular chordae 
E) Placement of  leads in a commissure


Answer:  E

Tricuspid Regurgitation continues to fumble cardiologists/physicians as any damage to tricuspid valve (TV) can be irreversibly catastrophic. Literature is ripe with debate on repair vs replacement of TV, as even a minor difference in clinical judgement can have a long-term trajectory effect. All of the above choices can increase or cause (TR) except choice E.

Actually one of the ways to avoid damage to TV is to secure placement of leads in a commissure, at a place outside the valve annulus, or replacement with epicardial leads.

References:

1. Al-Mohaissen MA, Chan KL. Prevalence and mechanism of tricuspid regurgitation following implantation of endocardial leads for pacemaker or cardioverter-defibrillator. J Am Soc Echocardiogr 2012; 25:245. 

2. Mazine A, Bouchard D, Moss E, et al. Transvalvular pacemaker leads increase the recurrence of regurgitation after tricuspid valve repair. Ann Thorac Surg 2013; 96:816. 

3. Molina JE, Roberts CL, Benditt DG. Long-term follow-up of permanent transvenous pacing systems preserved during tricuspid valve replacement. Ann Thorac Surg 2010; 89:318.

Q: Oxygen works as an afterload reducer for right-sided heart failure in cor pulmonale? 

 A)True 
 B) False


Answer:  A

Oxygen therapy acts as a reversal against vasoconstriction secondary to hypoxemia. Subsequently, it decreases pulmonary artery pressure. In fact, oxygen is considered as a drug of choice for pulmonary hypertension secondary to COPD/Cor pulmonale. 


References: 

1. Weitzenblum E, Sautegeau A, Ehrhart M, et al. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985; 131:493. 

2. Hoeper MM, Andreas S, Bastian A, et al. Pulmonary hypertension due to chronic lung disease: updated Recommendations of the Cologne Consensus Conference 2011. Int J Cardiol 2011; 154 Suppl 1:S45.

Sleep in ICU

(A relatively less discussed issue in ICU - sleep pattern in critically ill patients)

 "....it is possible that the modern critical care experience—including acute illness, a nontherapeutic environment for sleep and wakefulness, and exposure to multiple medications affecting neurotransmitter balance—engenders new sleep disturbances that persist in some subjects after intensive care. This is similar to the development of new or worsening cognitive function after critical illness and reflects shared mechanisms in the brain. Thus, there is a need for well-designed prospective studies that characterize sleep and circadian disruption throughout critical illness and recovery while examining their relationship to long-term neuropsychiatric outcomes."


Read:  Sleep in the Intensive Care Unit - A. Pisani & Coll. - American Journal of Respiratory and Critical Care Medicine Home -  Vol. 191, No. 7 | Apr 01, 2015


weblink: http://www.atsjournals.org/doi/full/10.1164/rccm.201411-2099CI

Q; Which of the following part of the gastrointestinal tract is more prone to stress ulceration in first few days of ICU admission?

A) Fundus and body of the stomach
B) Antrum
C) Duodenum
D) Distal esophagus
E) Colon


Answer:  A 

Stress ulceration in first few days of ICU admissions tends to occur in the proximal regions of the stomach. But, stress ulcerations that develop later during the intensive care hospitalization tend to be more distal and deeper.



References: 

1.  Shuman RB, Schuster DP, Zuckerman GR. Prophylactic therapy for stress ulcer bleeding: a reappraisal. Ann Intern Med 1987; 106:562. 

2. Cook DJ, Griffith LE, Walter SD, et al. The attributable mortality and length of intensive care unit stay of clinically important gastrointestinal bleeding in critically ill patients. Crit Care 2001; 5:368. 

3. DePriest JL. Stress ulcer prophylaxis. Do critically ill patients need it? Postgrad Med 1995; 98:159. 

4. Terdiman JP, Ostroff JW. Gastrointestinal bleeding in the hospitalized patient: a case-control study to assess risk factors, causes, and outcome. Am J Med 1998; 104:349.

Q; Intra Aortic Balloon Pump (IABP) decreases afterload via

A) a vacuum effect
B) Increasing blood supply to mesenteric vessels
C) Inflating Aortic diameter
D) Increasing blood supply to carotid arteries
E) Increasing blood supply to Right subclavian artery


Answer: A

Basic principles of IABP are unchanged since its clinical introduction. Two major effects of IABP are

1.  During inflation of IABP in diastole of heart cycle, blood is displaced to the proximal aorta 
2.   During deflation of IABP in systole of heart cycle, aortic volume, i.e afterload reduction occurs via a vacuum effect (created by rapid balloon deflation).



 Reference: 

 Weber KT, Janicki JS. Intraaortic balloon counterpulsation. A review of physiological principles, clinical results, and device safety. Ann Thorac Surg 1974; 17:602.

Q: When all measures fail in acute exacerbation of idiopathic Pulmonary Fibrosis (AE-IPF), lung transplant should be pursue aggressively as a last resort of salvage therapy..

A) True
B) False


Answer: B

Lung transplantation in IPF has sown good outcome only if its done as an elective process. It should not pursue as a salvage therapy in AE-IPF. It carries a very high mortality rate. Lately, some centers are using extracorporeal membrane oxygenation (ECMO) as a bridge to transplant (BTT) in AE-IPF, but data is still very thin. Ideally, all patients with IPF should undergo transplant evaluation while they are clinically at their baseline.


Reference: 

 Yusen RD, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: Thirty-second Official Adult Lung and Heart-Lung Transplantation Report--2015; Focus Theme: Early Graft Failure. J Heart Lung Transplant 2015; 34:1264.

Q: What is Phlebosclerotic colitis?


Answer: Phlebosclerotic colitis is a  form of ischemic colitis that results from venous obstruction, usually involving right side of the colon. It is hallmarked by fibrotic sclerosis and calcification of the walls of the mesenteric veins. It can be diagnosed or at least suspected on plain films (KUB), if linear calcifications are seen in the region of the right colon. Diagnosis can be confirmed by CT scan, with colonic wall thickening and mesenteric venous calcifications. This is usually self-limiting and resolve spontaneously, only requiring supportive treatment.


Reference:

Jan YT, Yang FS. Phlebosclerotic colitis. J Am Coll Surg 2008; 207:785.

Q: How lupus and antiphospholipid syndrome (APS) can be differentiated from Heparin Induced Thrombocytopenia (HIT)?


Answer: 

1. Lupus usually causes only mild thrombocytopenia and  almost never drops platelet count below  50,000/microL. Moreover, lupus-associated antiplatelet antibodies do not activate platelets and do not cause thrombosis.

2. APS,  like HIT can cause arterial and venous thrombosis but can be differentiated  from HIT

• by interaction of APS antibodies with phospholipids i.e cardiolipin and ß2-GP-I
• prolongation of the aPTT
• Platelet count almost never dropping below 50,000/microL

Q: Calculation of Pulmonary vascular resistance requires all of the followings except?

A) Central Venous Pressure (CVP)
B) Mean Pulmonary Artery Pressure (mean Pap)
C) Pulmonary capillary wedge pressure (PCWP)
D) Cardiac Output (CO)
E) Constant 80


Answer: A

Formulae for Systemic vascular resistance (SVR) and Pulmonary vascular resistance (PVR) is almost same except as SVR represent systemic circulation, it takes into account of CVP and MAP (Mean arterial Pressure). And, as PVR represents only pulmonary circulation, it takes into account of PCWP and mean-Pap instead of CVP and MAP respectively.

SVR = 80x [MAP – CVP]/CO)

PVR = 80 x [mean Pap – PCWP]/CO)

Q: Cirrhotic cardiomyopathy is usually due to

A) Secondary to underlying ETOH abuse
B) Itself is a primary disease
C) Due to hypoalbunemia of cirrhosis 
D) Due to frequent sepsis in cirrhosis
E) Due to Budd-Chiari Syndrome


Answer:  B 

 Cirrhotic cardiomyopathy is an independent disease found in cirrhosis. It is different from alcoholic cardiomyopathy. It is least understood of all cardiomyopathies. It is kind of a diagnosis of exclusion manifested as impaired contractile responsiveness to stress and/or diastolic dysfunction. Electrical abnormalities include QT interval prolongation, electrical and mechanical dyssynchrony, and chronotropic incompetence. One of the hallmark is the dilated left atrium but normal LV cavity size in most cases.


References: 

1.  Milani A, Zaccaria R, Bombardieri G, et al. Cirrhotic cardiomyopathy. Dig Liver Dis 2007; 39:507. 

2. Møller S, Henriksen JH. Cirrhotic cardiomyopathy. J Hepatol 2010; 53:179. 

3. Zardi EM, Abbate A, Zardi DM, et al. Cirrhotic cardiomyopathy. J Am Coll Cardiol 2010; 56:539.

4. Timoh T, Protano MA, Wagman G, et al. A perspective on cirrhotic cardiomyopathy. Transplant Proc 2011; 43:1649.

TTM in TH

Q; Recently for Therapeutic Hypothermia, 36°C for 24 hours has been recommended for otherwise non-complicated patient in coma after cardiac arrest. In which situations still lower temperature at 33°C for 24 hours is recommended?

Answer:  Studies have shown similar outcomes in non-complicated patients with either 36°C or 33°C for 24 hours. 

36°C is sufficient for patients 

• in coma but still, exhibit some motor response, 
• no malignant EEG patterns,  
• no cerebral edema 

Otherwise 32°C to 34°C should be applied for patients 

• in deep coma
• EEG c/w seizure
• cerebral edema

References:

1. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med 2013; 369:2197.

2. Arrich J, Holzer M, Havel C, et al. Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev 2016; 2:CD004128.

Mayo Clinic criteria for Takotsubo cardiomyopathy

Q: Diagnosis of Takotsubo cardiomyopathy (broken-heart syndrome) includes all of the following except?

A) Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture
B) Regional wall motion abnormalities typically in a single coronary distribution
C) Presence of EKG abnormalities
D) Troponin elevation
E) Absence of pheochromocytoma or myocarditis.


Answer:  B

Mayo Clinic diagnostic criteria 1 requires all of the following four criteria for the diagnosis

1. Transient left ventricular systolic (LV) dysfunction, which is typically regional and extend beyond a single epicardial coronary distribution*
2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture^
3.  New EKG abnormalities (e.g ST elevation or T wave inversion) or some elevation in cardiac troponin. 
4. Absence of pheochromocytoma or myocarditis.

*rare exceptions within one coronary distribution and the global type have been reported.
^ If coronary disease is found, the diagnosis of stress cardiomyopathy can still be made if the wall motion abnormalities are not in the distribution of the coronary disease 2



References:

1. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 2008; 155:408. 

2. Templin C, Ghadri JR, Diekmann J, et al. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med 2015; 373:929.

Q: What is the half-life of transfused cryoprecipitate?

Answer:  Half-life of transfused cryoprecipitate is about two to four days.

Fresh-Frozen -Plasma is thawed at 4°C for about 24 hours, which makes precipitates of cold-insoluble proteins, which are very rich in blood coagulation factors. This product can be kept frozen at -18°C for about one year to use for clinical transfusions. After transfusion, it is effective for about 2-4 days.

BNP and MR

Q: What is the clinical significance of  Brain Natriuretic Peptide (BNP) in Mitral Regurgitation (MR)?


Answer:   Unlike exacerbation of congestive heart failure (CHF), BNP in MR is more of prognostic value and reflection of the clinical outcomes rather than the severity of MR. Interestingly, it is an independent predictive value of mortality with adjustment to all other risk factors including low ejection fraction.

To be of surprise, serum BNP level just more than 31 pg/mL predicts lower five-year survival. Moreover, it also predicts poor outcomes after mitral valve surgery.


Reference:

1. Magne J, Mahjoub H, Pierard LA, et al. Prognostic importance of brain natriuretic peptide and left ventricular longitudinal function in asymptomatic degenerative mitral regurgitation. Heart 2012; 98:584. 

2. Hwang IC, Kim YJ, Kim KH, et al. Prognostic value of B-type natriuretic peptide in patients with chronic mitral regurgitation undergoing surgery: mid-term follow-up results. Eur J Cardiothorac Surg 2013; 43:e1. 

3. Perreas K, Samanidis G, Dimitriou S, et al. NT-proBNP in the mitral valve surgery. Crit Pathw Cardiol 2014; 13:55.

Q: What is the most common site of wall usually involved in the dissection of ascending aorta?



Answer: The most common site of wall usually involved in the dissection of ascending aorta is the right lateral wall.


Reference:

Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 1984; 53:849.

Q: Foley catheter balloon should be inflated with (select one)

A) Sterile water 
B) Normal Saline 


Answer: Sterile water

Foley catheter balloon should be inflated with sterile water (after urine flow is confirmed). Normal Saline should never be used to inflate the Foley catheter balloon because it may cause crystal formation, obstruct the balloon channel and later prevent the deflation of balloon.


Reference:

Daneshmand S, Youssefzadeh D, Skinner EC. Review of techniques to remove a Foley catheter when the balloon does not deflate. Urology 2002; 59:127.

Hypoxia in drowning

Q: What is the recommended oxygen saturation in a post drowning patient? 

 A) 88% 
B) 90% 
C) 92% 
D) 94% 
E) 100%

Answer: D (94%)

In post drowning patients higher than normal pulse-ox saturation or PO2 (60 mmHg) is recommended as tissue hypoxia is the major cause of the fatality. While managing hypoxia in post drowning patient, at least three points should be kept in mind

• There should be a low threshold for intubation and beside hypoxia, even mild to moderate hypercarbia requires intubation at PCO2 50 mmHg (some even suggests more than 45 mm Hg)
• In comparison to other patients, the orogastric tube is almost mandatory in post drowning patients as gastric distension may hamper ventilation.
• Positive pressure ventilation (PPV) with higher PEEP is recommended but it comes with its own price in post drowning patients, as the line of demarcation between hypotension due to PPV and therapeutic oxygenation is very thin, and requires particular monitoring post intubation.

Reference:

Layon AJ, Modell JH. Drowning: Update 2009. Anesthesiology 2009; 110:1390.

Q; In patients with a history of alcohol abuse which three vitamins required to be replaced on relatively urgent basis after admission?

Answer:

• Thiamine 100 mg daily, 
• Vitamin B6 2 mg daily, and 
• Folic acid 1 mg daily

Another difference between other patients and patients with ETOH abuse is, they require frequent feedings, with the goal of an energy intake of 35 to 40 kcal/kg of body weight/day and protein intake of 1.2 to 1.5 g/kg of body weight/day.


Reference: 

The European Society for Clinical Nutrition and Metabolism (ESPEN). ESPEN Guidelines. http://www.espen.org/espenguidelines.html 

Q: In patients with Aplastic Anemia transfusions should only be given from close family members?

A) True 
B) False

Answer: B (False)

Ideally, patients with Aplastic Anemia should not receive blood product transfusions from a sibling or a family member, to minimize the risk of an immune reaction to donor antigens, as in the case of Hematopoietic Cell Transplantation (HCT), which may lead to graft failure.

Q: In otherwise routine cases, which part of the kidney is usually targeted for biopsy?



Answer: Lower pole

Kidney Biopsy is usually performed with patient in prone position with pillow underneath, and under ultrasound. The lower pole is targeted  as it minimize the chances of hitting any major vessel.




References:

1. Korbet SM. Percutaneous renal biopsy. Semin Nephrol 2002; 22:254.

2. Whittier WL, Korbet SM. Renal biopsy: update. Curr Opin Nephrol Hypertens 2004; 13:661.

3.  Korbet SM, Volpini KC, Whittier WL. Percutaneous renal biopsy of native kidneys: a single-center experience of 1,055 biopsies. Am J Nephrol 2014; 39:153.

5. Shidham GB, Siddiqi N, Beres JA, et al. Clinical risk factors associated with bleeding after native kidney biopsy. Nephrology (Carlton) 2005; 10:305.

6. Wiseman DA, Hawkins R, Numerow LM, Taub KJ. Percutaneous renal biopsy utilizing real time, ultrasonic guidance and a semiautomated biopsy device. Kidney Int 1990; 38:347.

Q: How far cuff of endotracheal tube should be placed to prevent vocal cord palsy?


Answer:  At least 15 mm below the vocal cords

Vocal cord palsy is an undesired, though rare  but a serious complication of endotracheal intubation. The anterior branch of recurrent laryngeal nerve traverses between the lamina of thyroid cartilage and laryngeal mucosa. Overinflated cuff of ET-Tube may compress to cause vocal cord paralysis. First 10 mm of the area below vocal cord is most sensitive for damage. Ideally, ET-tube cuff should be at least at 15 mm below the vocal cords.



Reference: 

Benumof JL, Saidman J, editors. 2nd ed. London: Mosby; 1999. Anesthesia and Perioperative Complications; p. 9.

Q: What one advantage urinary trypsinogen activation peptide (TAP) has over amylase and lipase in acute pancreatitis? 

Answer: Trypsinogen activation peptide (TAP) is a five amino-acid peptide elevated in acute pancreatitis. It is cleaved from trypsinogen to become active trypsin. Though it may only be of academic interest but it is one of the earliest marker of acute pancreatitis, as well as it co-relates with severity of acute pancreatitis.


References: 

1. Tenner S, Fernandez-del Castillo C, Warshaw A, et al. Urinary trypsinogen activation peptide (TAP) predicts severity in patients with acute pancreatitis. Int J Pancreatol 1997; 21:105. 

2. Khan Z, Vlodov J, Horovitz J, et al. Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis: a prospective study. Am J Gastroenterol 2002; 97:1973.