Medical Management of Abdominal Compartment Syndrome

Medical Management of Abdominal Compartment Syndrome

An elderly man was admitted after a Hartman’s procedure with primary closure for a perforated sigmoid diverticulum with four quadrant peritonitis. Postoperatively, he remained ventilated and noradrenaline dependent. His intra-abdominal pressures gradually rose from 15 to 24mmHg. Urine output was poor, and he required peak pressures of 28cmH2O to achieve 6ml/kg tidal volumes. Vasopressor requirements gradually increased and a diagnosis of abdominal compartment syndrome was made. Medical management was attempted with fluid resuscitation, increased sedation, aspiration of nasogastric tube and neuromuscular blockade. However this did not improve the intra-abdominal pressures so the patient returned to theatre laparostomy and VAC dressing. On return from theatre, intra-abdominal pressures stabilised between 12 and 15mmHg. Noradrenaline requirements fell and urine output improved. The abdomen was closed on day 5 and he was discharged from ICU on day 10.

What non-surgical strategies can be used to reduce intra-abdominal pressure?

Read More »

Hypertonic Saline for Raised Intracranial Pressure

Hypertonic Saline for Raised Intracranial Pressure

A 40 year old male was brought into ED following a high speed road traffic accident. The patient was ejected from the vehicle. The patient was managed according to ATLS guidelines. He suffered extensive injuries including facial fractures, traumatic subarachnoid haemorrhage and multiple intra-cerebral haemorrhages, a flail chest and thoracic and cervical spine injuries. Once stabilised, the patient was transferred to the neurosurgical intensive care unit where an intra-cranial pressure (ICP) monitor was inserted to measure intracranial pressures. His ICP was persistently raised despite optimising respiratory parameters, deep sedation, muscle relaxation and then mannitol. A decision was made to commence an infusion of hypertonic saline 2.7% according to the local protocol. The ICP improved rapidly and stabilised and removed the need to proceed with surgical decompressive craniotomy.

What is the evidence for the use of hypertonic saline in the treatment of acutely raised intracranial pressure?Read More »

Neuroprognostication Post Cardiac Arrest (Post TTM Era)

Neuroprognostication Post Cardiac Arrest (Post TTM Era)

A  young adult female with known diagnosis of poorly controlled type 1 diabetes mellitus was admitted with out-of-hospital cardiac arrest. She had only recently been discharged from hospital after an admission with diabetic ketoacidosis. On arrival she had a GCS 3 with minimal respiratory effort. She was in profound DKA. Her temperature was 34.7°C on admission to ICU and she had targeted temperature management aiming for 36°C which was achieved within 2 hours. Her pH had normalised to 7.35 within 8 hours. 48 hours later one pupil became fixed and dilated. CT brain was consistent with global hypoxic ischaemic injury. EEG and SSEP on day 3 revealed severe lack of normal cortical activity. After discussion with family, treatment was withdrawn on day 4.

How do we undertake neuroprognostication after cardiac arrest in the post-TTM era?

Read More »

Corticosteroids in Septic Shock

Corticosteroids in Septic Shock

A week after an elective colectomy, a 70yr old man developed septic shock and multiorgan failure secondary to anastomotic breakdown. He was managed according to surviving sepsis guidelines with source control, early antibiotics, fluids and noradrenaline. The patient remained hypotensive and refractory to noradrenaline therapy, and had vasopressin and low dose hydrocortisone infusion commenced.

What is the evidence for the use of corticosteroids in septic shock?Read More »

Heparin Induced Thrombocytopenia

Heparin Induced Thrombocytopenia

A 62 year old lady with a metallic aortic valve was admitted to the cardiac unit for urgent surgical repair of a severely regurgitant mitral valve. He was normally on warfarin for his metal valve. This was stopped and unfractionated heparin commenced on day 4 once his INR level had dropped below the therapeutic range. The patient’s platelet count was 147*10^9/L on admission. By day 4 it had dropped to 85*10^9/L. After heparin was started it dropped further to a nadir of 55*10^9/L on day 8.

Could this be due to heparin induced thrombocytopenia? What investigations are required and how should we treat it?
Read More »

Hepatorenal Syndrome

Hepatorenal Syndrome

A 54 year old man with a history of alcohol excess was admitted under the medical team with an upper gastro-intestinal bleed. He had a background of pulmonary fibrosis that limited his exercise tolerance to 30 yards. Antibiotics, terlipressin and fluid resuscitation, including blood, were given. An oesophago-gastro-duodenoscopy demonstrated severe portal gastropathy but no active bleeding or varices. An abdominal ultrasound demonstrated cirrhosis and some moderate ascites. On day two of the patient’s hospital admission he was admitted to the intensive care unit (ICU) with respiratory failure and non-invasive ventilation was started. Over the next few days his condition deteriorated and he required vasopressor support. By day 6 the patient was oliguric, and his creatinine had risen from 102 to 155 µmoles/l.

What is the cause for his acute kidney injury? Could it be hepatorenal syndrome? Read More »

Hypertriglyceridaemia Induced Acute Pancreatitis

Hypertriglyceridaemia Induced Acute Pancreatitis

A young man is admitted to the surgical unit with several months of worsening abdominal pain. It has become much more severe over the last 24 hours. A CT scan shows evidence of acute pancreatitis with no gallstones or biliary duct dilatation.. He is normally well with no history of alcohol excess. His triglyceride level is elevated at 83.7mmol/L and a diagnosis of hypertriglyceridaemia induced acute pancreatitis is made. 

What is hypertriglyceridaemia induced acute pancreatitis and how is it treated?

Read More »

Therapeutic Hypothermia after Cardiac Arrest (Post-TTM)

Therapeutic Hypothermia after Cardiac Arrest (Post-TTM)

A 55 year old presented to ED following a witnessed VF arrest. He received bystander CPR and several shocks from the ambulance crew. He was intubated at the scene, and transferred to ED with return of spontaneous circulation. He had primary PCI to LAD and was transferred to the ICU for therapeutic hypothermia. He was kept at 33 degrees for 24 hours, and rewarmed over 8 hours. He extubated 2 days late with no cognitive impairment, and mild weakness in one arm.

What is the evidence for and against Targeted Temperature Management (TTM) post cardiac arrest?Read More »

Transfusion in Sepsis

Transfusion in Sepsis

A 85 year old man presented with acute bowel obstruction. He had a history of hypertension and diverticulitis disease, but was active for his age. He was not known to have coronary or any other vascular pathology. At laparotomy, a large diverticulitis abscess was identified. When this was manipulated, he developed an SVT with a ventricular rate of 210 bpm which progressed to VT. He received 1 mg adrenaline and 2 minutes CPR in total, with no electrical shocks. At this point perfusion and pressure returned. Surgery was expedited and simplified. He remained intubated and ventilated on ITU post-operatively. ECG demonstrated global t-wave inversion. He required noradrenaline and adrenaline to maintain blood pressure. During the initial 48 hours, his haemoglobin (Hb) fell from 11.9 g/dl to 8.1 g/dl, raising the suggestion of packed red cell (PRC) transfusion.

What is the most appropriate threshold to transfuse packed red cells in critically ill patients?Read More »

Tranexamic Acid in Trauma

Tranexamic Acid in Trauma

A 19 year old man experienced a head on collision as the driver of a car. He suffered significant lower limb open fractures, pelvic fractures, lung injuries and a small subarachnoid bleed. Initial management was performed in ED and included oxygen, IV access and fluid, lower limb and spine immobilisation, and analgesia. He underwent a trauma series CT scan, which identified the various injuries given above. At no point was his level of consciousness a concern, and he maintained his own patent airway throughout. He did not show signs of haemodynamic instability or evidence of life threatening haemorrhage. Tranexamic acid (TXA) was not given.

What is the evidence for using tranexamic acid in trauma?

Read More »