Category Archives: Abdomen

Critical Care Refresher Course: Trauma and Surgery

GI Bleed (Kumar)

What is a massive GI bleed?

  • Bleeding resulting in CVS collapse
  • mortality up to 40%
  • over 75% due to upper GI bleed (lower GI bleed mortality 2%)

Etiology

  • Ulcers (Duodenal > Gastric)
  • Gastritis
  • Varices
  • Oesophagitis

Team: Gastroenteritis, Surgeon, Interventional Radiologists

Pharmacotherapy

Acute pancreatitis (Marshall)

Pancreatitis is a chemical burn of the retroperitoneum

Incidence 10-80/100,000

Mortality 10-25%

Pathophysiology

  • Fluid collection, ascites
  • Pseudocyst
  • Fat necrosis

Severity scores –

Resist antibiotics

No other intervention except PATIENCE!

Early surgery for pancreatitis do badly.

How to feed the critically ill – Dr James Day

Why is hypocaloric feeding better- Casear

Doesn’t kill nor saves lives

May avoid infections and enhance recovery

Doesn’t compromise recovery

Reduction of ICU acquired weakness

Early nutrient restriction and hypocalorific feeding are harmless and may enhance recovery

Early nutrient restriction avoids early suppression of autophagy in skeletal muscle

The optimal duration of nutrient restriction and role of different macro nutrients needs to be further eleucidated

Should autophagy be respected or activated?

 

References

EPaNIC Study

Review: Timing of PN

CALORIES trial

 

Feeding and Chronically Critically ill-Guttormsem

What does chronically critically ill mean:

  • Presence of tracheostomy
  • On ICU>7 days

Unresolved issues:

  • How much energy to give?
  • Hypocaloric or isocalorific- different targets in different phases of the ICU/hospital stay

How much protein to give- need to see energy, protein and muscle as unity.

Is it possible to identify the critically ill patient at nutritional deficiency?

Energy demands may double in the rehabilitation phase of critical illness. They are back on the ward then.

When pt out of bed (i.e. rehabilitation phase) feed to put on weight (muscle mass)

 

References:

The evolution of nutrition in critical care: how much, how soon?

 

What to do when there is no EBM?

Septic patients (Perel)

EBM de-emphasises intuition, unsystematic clinical experience & pathophysiological rationale as sufficient grounds for clinical decision making & stresses the examination of evidence from clinical research

No benefit to ARISE, PROCESS, PROMISE

Have multimodal approach to monitoring the CV system of septic patients

Solve therapeutic conflicts by choosing the least harmful option

Aim to de-escalate treatment as soon as possible and do not aim to normalise values

 

References:

Positive fluid balance in septic patients

A protocol-less approach to septic patient

 

The High Risk Surgical Patient (Zsolt)

References

EuSOS study

Pro-AQT study

OPTIMISE Study

Choice of monitoring device amongst anaesthetists

No benefits of SV optimisation in elective abdo surgery

 

Liver Failure (Wendon)

EASL Practical guidelines for the management of alcoholic liver disease

EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis

Hepatorenal syndrome: the 8th international consensus conference of the Acute Dialysis Quality Initiative (ADQI) Group

 

Subarachnoid Haemorrhage (Polderman)

Unsecured aneurysms rebleed 9-17% on day 0

Fever associated with poor outcomes

High incidence of CV dysfunction. Therefore would advocate CO monitoring

References

Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference.

 

Critical Care Refresher Course: Abdomen

Acute Liver Failure (Rothen)

Grades of hepatic encephalopathy

  • Grade 1 – Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction
  • Grade 2 – Lethargy or apathy; minimal disorientation for time or place; subtle personality change; inappropriate behaviour
  • Grade 3 – Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation
  • Grade 4 – Coma

Acute liver failure is a multisystem disorder – hepatic damage leads to endotoxemia –> MODS

Mechanism of drug-induced hepatic damage – idiosyncratic (immune and non-immune) or toxic

Paracetamol may be used in non-paracetamol related liver injuries

Cerebral oedema occurs in up to 75% of pts with grade 4 encephalopathy

  • lactulose and rifaximine in ALF controversial

In absence of bleeding or invasive procedures in unnecessary

Prophylactic antibiotics is controversial

Prognosis is improving although it is highly dependant on the underlying aetiology

 

References

NEJM Review of acute liver failure

Aetiology of acute liver failure

Liver toxins database

Paracetamol toxicity

Management of acute liver injury

Review and King’s criteria for liver failure

 

 

Chronic Liver Diseases and Transplantation (Wendon)

Key to management is the aetiology

CT WITH contrast, US and Echo should be standard investigation in the cirrhotic patient

Organ issues

  • Cardiac – cirrhotic cardiomyopathy, impaired response to stress, diastolic dysfunction, Pulmonary hypertension
  • Renal – true hepatorenal syndrome is rare; the cause is often multifactorial. Creatinine is a very poor marker of renal impairment in liver failure. Treatment – consider terlipressin and albumin
  • CNS – encephalopathy increases ITU stay and mortality. Management – care of airway, no evidence for protein, consider precipitant and treat. MARS device has no
  • Infection
  • Varices – not all pts with varices have cirrhosis. Restrictive Hb strategy. TIPS early
  • Coagulation – pts have balanced coagulation as they also have low ATIII, protein C and S
  • Respiratory – hepatopulmonary syndrome. SHUNT!

Propofol and clonidine sedative of choice in liver failure. Small bolus opioids.

References

Lancet: Review of liver cirrhosis

Hyponatraemia and cirrhosis

Acute vs acute-on-chronic liver failure

Early use of TIPS

CANONIC Study

 

Liver Surgery (Sitzwohl)

Liver resection is increasing; metastases (majority), primary liver tumour, benign lesions

Mortality improving – 2% BUT complication 20-30%

Major complications – SEPSIS, wound infection

Fluids – less is more; CVP has direct effect on blood loss

Coagulation – abnormal lab values DO NOT predict bleeding risk = BALANCED COAGULATION. Aprotinin and transexamic acid is of uncertain value in these patients.

Sedation – NOT Midazolam. Cautious Dexmedetomidine. NOT Morphine. Bravo Remifentanil. Yes Propofol

Modified eFAST scan is useful in liver transplant patients to look for free fluid

 

References

Morbidity and mortality after liver surgery

CVP and liver resection

Renal failure after liver transplants

Probiotics in liver transplant