COM acute pancreatitis answers: Question 1a&b

Clinical features, diagnosis and investigation of acute pancreatitis

Further stratification of a differential diagnosis can be sought on enquiry or identification of risk factors for each particular condition and examination of the patient.  In this case an ERCP within the last 24hours puts pancreatitis at the top of this patient’s differential diagnosis of epigastric pain. 

Typical clinical features of acute pancreatitis include moderate to severe epigastric pain radiating to the back often relieved by sitting forward.  Usually there is vomiting and examination will reveal a tender epigastrium with some guarding and the patient may even be pyrexic, diaphoretic and tachypnoeic depending on the degree of systemic inflammatory response syndrome and any organ failure present.

Laboratory investigations and imaging are important in both confirmation of pancreatitis but also in the stratification of disease severity and the assessment of its local or systemic complications. 

Diagnosis by detecting an elevation of serum amylase or lipase concentrations depends on at what point, in the clinical course, the patient presents to hospital. A plasma amylase greater than three times the upper reference limit is usually diagnostic for acute pancreatitis.  But in delayed presentations or chronic pancreatic exocrine insufficiency levels may not be significantly raised.  Amylase begins to rise in the first twelve hours and only remains elevated for three to five days.  In cases of delayed presentation, serum lipase levels remain elevated for eight to fourteen days. The British Society of Gastroenterology guidelines recommend that a diagnosis of acute pancreatitis should be made within 48hours and that where readily available; serum lipase is the preferred test.  In cases of doubt imaging can be used to help with diagnosis and CT abdomen with IV contrast is the investigation of choice but this is generally used for assessment of severity and intra-abdominal complications.  Some other texts suggest the use of urinary enzymes in the diagnosis but given the availability of other tests and imaging to help with diagnosis urinary tests are not widely used.

Disease severity and prognosis can be gauged using both clinical features, laboratory variables and imaging findings.  Ranson, Imrie (Glasogow) and APACHE II are multivariable scores while CRP (>150mg/l) is the single most sensitive marker and the Balthazar criteria use imaging to assess appearance of the pancreas and extent of necrosis in indicating the severity of acute pancreatitis.

When assessing severity of pancreatitis it is important to draw a distinction between actual and predicted severe pancreatitis.  Actual severe pancreatitis is defined by the Atlanta criteria as that which is associated with persisting organ failure or local complications such as pseudocyst, necrosis, or abscess.  However, these criteria are outdated and definitions of the local complications have evolved since their inception. There are no currently updated international consensus guidelines on the definition and prediction of severe pancreatitis however the BSG recommend using patients clinical state, CRP multivariate score at 48hrs to assess severity.  CT is not routinely used early in pancreatitis but is obviously employed if the patient’s clinical state requires further investigation.

COM: Acute Pancreatitis Question 2 (CABS) Answer

Clinically applied anatomy for imaging

CT abdomen is commonly used to assess patients with acute pancreatitis for any complications such as necrosis or pseudocyst formation.   A radiologist usually reports the scans but it is professionally essential that a doctor have enough knowledge of gross anatomy to view the scans and understand the report to convey information to the patient and other healthcare professionals in an appropriate manner.

The pancreas is a retroperitoneal structure at the level of L1/L2 intimately related to the duodenum, common bile duct and major vessels of the systemic and portal circulation, left kidney and spleen.  With four main parts the pancreas is an elongated organ with a comma shaped uncinate process and head that travels superiorobliquely   as an elongated body and tail to the splenic hilum.  All four parts of the U-shaped duodenum are applied to the pancreas but the main pancreaticobiliary duct opens in to the second part of the duodenum via the ampulla of vater. This is clinically very relevant for those perfoming an ERCP. 

Abdominal aorta and inferior vena cava both lie posterior to the pancreas while the coeliac trunk, superior mesenteric artery, and portal vein with its tributaries coarse in and around the pancreas.  The superior mesenteric vessels travel posterior to the head and body of the pancreas and anterior to the uncinate process and duodenum in a nutcracker arrangement.  This intimate vascular relationship to the pancreas often makes resection of pancreatic tumours impossible due to the anatomical difficulty and risk when tumour involves a major vessel.

Anterior to the pancreas is the lesser sac, stomach and transverse colon with the spleen and left kidney related laterally and posteriorly, respectively.  

In transverse section, as is the case with CT imaging, the anatomy can be identified by relation to the above land marks and any abnormality in size, shape or attenuation particularly the appearance of air or fluid should be noted. If unsure as to the nature of any decreased attenuation air can also usually be seen elsewhere in the GI tract for comparison.

COM AP: Q3 Answer

Prognostication

COM acute pancreatitis: Q4 answers

Aetiology

All of the aetiological groups in the table below can cause pancreatitis. In up to 80% of cases an underlying aetiology should be found with up to 50% related to gallstone disease and 20 – 25% related to alcohol misuse and the remaining small percentage related to the other identifiable causes listed in the table below. Around 20% of cases are diagnosed as idiopathic.

The table above includes examples of less common causes of acute pancreatitis.  Those most relevant to clinical practice are highlighted in bold and further investigation is commonly directed at identifying or managing such causes.   

COM acute pancreatitis: Q5 answers

(a)Complications: Pleural effusions

Pancreatitis can be accompanied by an acute peripancreatic fluid collection within the first 48hrs, necrosis, pseudocyst or even haemorrhage. Although the natural history of the latter three complications tends to evolve over a time frame of weeks rather than days and haemorrhage usually only occurs in those undergoing necrosectomy.  

Outside the abdomen, pleural effusions are also common in acute pancreatitis and as outlined below severe pancreatitis will cause SIRS and potentially lead to multiorgan dysfunction syndrome (MODS).  The patient should be assessed comprehensively using and A-E approach as there are other potential causes of dyspnoea & tachypnoea in those who are acutely ill and life threatening medical problems, in addition to SIRS, such as MI or PE should be considered if the patient does not have effusions on clinical examination or chest x-ray or a recent CT scan.

(b)Complications: SIRS

Acute illness or injury results in an inflammatory response. The magnitude of this response can be so severe as to cause systemic upset with derangement of the patient’s respiratory and circulatory systems.  Pathophysiology is not discussed here but the clinical phenomenon is known as systemic inflammatory response syndrome (SIRS).  Clinical definition of SIRS outlined below was initially presented by Bone et al.  If SIRS is due to a proven or presumed infective insult then the term sepsis is used. Recent definitions and classification of sepsis and grading were published and the relevant terms are outlined below. 

• SIRS:  Systemic inflammatory response syndrome HR > 90, Body Temp <36^oC or >38^oC, respiratory rate >20 or arterial PaCo2 < 4.3kPa, WCC <4 or >12 or >10% immature neutrophils
• Sepsis: SIRS of presumed infective or proven infective origin
• Severe sepsis: Sepsis causing end organ dysfunction
• Septic Shock:: end organ dysfunction refractory to adequate fluid resuscitation
• MODS: altered function of multiple organs such that homeostasis cannot be maintained with out intervention

(c)Complications: Investigation of acutely unwell patients

All acutely ill patients should be assessed using the A-E approach.  In this setting it is important to determine the cause of respiratory compromise and determine if sepsis has supervened.  The two most important initial investigations are therefore blood cultures along with the usual bloods and simultaneous access for resuscitation and a portable chest x-ray.  Although, CT is not routinely performed within four days of presentation unless diagnostic uncertainty persists, it is now pertinent to rule out additional intra abdominal complications.  Senior colleagues will probably request a CT abdomen with IV contrast.

COM acute pancreatitis: Q6 answers

(a) Clinical pharmacology: Oral anticoagulation and drug & interactions

Vitamin K is an essential cofactor in the hepatic synthesis of clotting factors II, VII, IX, X, XI the action of which is measured by PT or INR assays. Patients who have obstructive jaundice do not absorb vitamin K and have elevated PT or INR.  Those who are malnourished such as this patient will also have reduced levels of Vitamin K therefore even the smallest amount of warfarin will have a profound effect on the INR.  This patient’s INR was difficult to control on minimal doses of warfarin therefore it was discontinued and coagulation monitored daily.  Once INR <2 therapeutic Enoxaparin was initiated but coagulation monitored closely.  Patient required anticoagulation for AF which became progressively less well controlled with more frequent degeneration to AF with a rapid ventricular response.  Review of the Kardex revealed a combination of β agonist and antagonist therapy.  COPD and AF are exacerbated by β antagonist and agonist therapy respectively. The effect of β agonist therapy was particularly pronounced as this patient was on a background long acting β agonist in addition to regular 2.5mg Salbutamol nebules.  β antagonist was changed to digoxin and the use of sulbutamol nebulas limited to the treatment of rhonchi on a PRN or acute basis.

(b) Clinical pharmacology: Drug and Electrolyte interactions of Antiarrhythmatics

In this situation the patients electrolytes must be checked urgently and any hypokalaemia or hypomagnesaemia corrected rapidly.  The potential dysrhythmic interaction between digoxin and hypokalaemia is also important in this situation.

References

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