Transplantation After Brainstem Death

A 38-year-old previously fit man suffered a grade five subarachnoid haemorrhage. Attempts at coiling failed and he suffered a catastrophic rebleed on-table whereupon his pupils became fixed and dilated. After a suitable sedation washout period he underwent testing which confirmed brainstem death at which point he was referred to the specialist nurse for organ donation. Following counselling of the family and appropriate assessment, donation of his kidneys, liver and heart was agreed.

Upon confirmation of brainstem death, mechanical ventilation was continued to ensure PaO2 greater than 10 kPa and limit peak inflation pressure to less than 30 cmH20. Vasoactive support was switched from noradrenaline to vasopressin 0.02 iu/kg/min. Methylprednisolone and intravenous triiodothyronine were administered whilst awaiting harvest. Blood antibody testing for HIV1+2, Hepatitis B and C, HTLV-1 and CMV IgG were all negative. A transthoracic echocardiogram confirmed good biventricular function; following discussion with the transplant retrieval team a pulmonary artery catheter was floated. Clinical measurements of cardiac output and mixed venous oxygen saturation were satisfactory. Adequate hydration was maintained with crystalloid by infusion and glucose control optimised in the range 8-10 mmol/L with insulin. The dedicated retrieval team performed the organ retrieval eighteen hours after confirmation of brainstem death.

How can we optimise organ function for organ donation?Read More »

Use of Bicarbonate in Lactic Acidosis

Five days post emergency colorectal surgery, an elderly woman, following a brief period of chest pain a few hours earlier, developed progressive hypotension and tachycardia on the ward. She had a background of hypertension, type 2 diabetes and a chronic left foot ulcer. On examination she was found to be clammy, mottled and peripherally vasoconstricted with a GCS of 15/15. Her abdomen was soft and non-tender. Her initial ECG had showed no ischaemic changes and subsequent ECGs showed only a sinus tachycardia.

Initial blood gas analysis showed a metabolic acidosis (pH 7.21 Lactate 2.8mmol/l, HCO3 11.1mmol/l with a pCO2 of 2.7kPa).  A starting differential diagnosis of a cardiac event, a pulmonary embolism, critical ischaemia or sepsis related to a hip or foot ulcer were made. Urgent orthopaedic and vascular review were obtained, and it was deemed that neither the hip, ulcer or vascular insufficiency were a likely source for the deterioration. Initially it was planned to transfer her for a CTPA, however she became progressively unstable, was no longer fluid responsive, and was intubated on the ward and transferred to the intensive care unit (ICU) for stabilisation.

On arrival on ICU she continued to deteriorate, and in addition to fluid resuscitation required a high dose noradrenaline infusion to maintain her blood pressure. Broad spectrum antibiotics were started, a bedside echocardiogram and blood tests performed and hydrocortisone started. Her metabolic acidosis continued to deteriorate, subsequent arterial blood gas showed a pH 6.91, Lactate of 13.7mmol/l, HCO3 7.7mmol/l, base excess -25mmol/l with a pCO2 of 5.4kPa. It was decided to correct this acidosis with a bicarbonate infusion and initially 200ml of 8.4% was given over an hour, based on correcting half the calculated bicarbonate deficit (bicarbonate deficit (mmol) = base deficit 0.3xbodyweight(kg)1).  The blood gas following this infusion showed improvement in the metabolic acidosis despite the increasing Lactate (pH 7.07, Lac 14.0mmol/l, HCO3 10mmol/l, BE -18.6mmol/l with a pCO2 of 4.85kPa). She continued to deteriorate and the results from her blood tests, troponin and bedside echo suggested a primary myocardial infarction to cause this decline. She was too unstable for primary coronary intervention and her condition continued to deteriorate. She died 6 hours post admission.

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Massive Transfusion in Upper Gastrointestinal Haemorrhage

A 55 year old male presented with acute upper abdominal pain and haematemesis. He had admitted drinking alcohol to excess. Following admission, he had a further significant episode of haematemesis associated with haemorrhagic shock. An emergency oesophagogastrectomy (OGD) was arranged in theatre. His pre-procedure haemoglobin was 60g/L.  OGD revealed large amounts of fresh blood in the stomach, which prevented identification of the bleeding point. The patient had a number of oesophageal varices, attempts were made to band these but this did not stop the bleeding. A partial gastrectomy was undertaken. The patient received a total of 18 units of red blood cells, 14 units of flesh frozen plasma and 2 units of platelets and cryoprecipitate before being taken to Intensive Care intubated and ventilated.

On the Intensive Care Unit he was warmed and repeat blood tests were sent to ensure correction of his coagulopathy. Haemoglobin was recorded as 9.4g/dL and the APTTr was normal. The following day when he was normothermic and cardiovascularly stable he was woken and extubated. He was discharged to the ward the following day.

When should we transfuse in upper gastro-intestinal haemorrhage? Are there any adjunctive therapies that can help?Read More »

Major Haemorrhage and Recombinant Factor VIIa Concentrate

Major Haemorrhage and Recombinant Factor VIIa Concentrate

A 40-year-old female intravenous drug user presented with a diffusely swollen right lower leg. She had injected heroin into her right thigh one week previously. The swelling started 3 days later. Initial observations revealed T 39.6, HR 135, NIBP 100/87, RR 32, Sats 96% on air. On examination, she was pale and sweaty. She had a swollen right lower leg with mottling of her foot and poor pedal pulses. Following initial fluid resuscitation, chest X-ray, cultures and broad-spectrum antibiotics (Flucloxacillin, Metronidazole and Gentamicin), she underwent CT angiogram of her lower limbs which showed oedematous and expanded muscle compartments of the thigh and calf but patent arterial flow to the feet. There was also right common femoral vein thrombosis with some vessel patency. Initial labs revealed neutrophilia (9.2), thrombocytopaenia (16) and deranged coagulation (PT 16, APPT 33, Fib 2.6). CK was 57000. She underwent right leg fasciotomies and was brought to ICU ventilated and on Noradrenaline to maintain MAP >65. She commenced Immunoglobulin IV 1gram/kg per day for 2 days for suspected Streptococcus Group A sepsis. That night she had massive transfusion requirements due to ongoing haemoserous ooze from her fasciotomy sites, losing up to 1 litre of haemoserous fluid per hour. Overnight she received 10 units RCC, 8 x FFP, 6 x Platelets and 2 x Cryoprecipitate, as well as Vitamin K (guided by Hb on ABG, formal lab results and thromboelastography). She was discussed with the Haematology Consultant and it was decided that, if rapid blood loss continued despite full correction of her clotting factors, fibrinogen and platelets then Factor VII could be given. However, over the next 2 hours, losses were much reduced following product replacement, and since she already had clot in her femoral vein, Factor VII Concentrate was not given.

What is the role of Recombinant Factor VIIa in major haemorrhage?

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Tourniquets in Severe Traumatic Limb Haemorrhage

Tourniquets in Severe Traumatic Limb Haemorrhage

A 30 year old male pedestrian was involved in a road traffic collision with a car travelling at speed. On arrival of the paramedics he was found to be unconscious with evidence of severe blood loss. He also had a partial amputation of his right leg below the knee. The paramedics applied a combat application tourniquet to the thigh, above the injury. He then suffered a cardiorespiratory arrest and CPR was commenced. On arrival in the emergency department his trachea was intubated and he underwent bilateral decompressive thoracostomies. Large bore intra-venous access was secured and two units of packed red cells given by a rapid infusion device. He remained haemodynamically unstable requiring a further six units of red cells and associated blood products to maintain a systolic blood pressure of above 80mmHg. Orthopaedic members of the trauma team were persistently keen to remove the tourniquet in order to prevent distal-neurovascular damage. This request was repeatedly denied and he was transferred rapidly to theatre for definitive control of his ongoing haemorrhage with an exploratory laparotomy. No cause for haemorrhage was found on laparotomy so attention shifted to damage control surgery on his leg in order to try and achieve some haemodynamic stability. Unfortunately to achieve this aim the tourniquet was removed. Bleeding was uncontrollable even with reapplication of the tourniquet and the patient exsanguinated and died.

What are the current recommendations for the use of limb tourniquets in trauma, and what is the evidence base for those recommendations?

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Rapid Response Systems

Rapid Response Systems

An elderly man was admitted with an acute abdomen and free air visible under the diaphragm on CXR. He was fluid resuscitated before undergoing emergency laparotomy, where a perforated duodenal ulcer was oversewn. He was admitted to ICU postoperatively, extubated the next morning and deemed fit for discharge to the surgical ward later that day. Due to a lack of surgical beds, he was eventually discharged from ICU at 22:30. Eight hours post discharge, he was urgently re-referred to ICU after being found moribund on the ward. Before he could be seen and assessed he suffered an unrecoverable asystolic arrest. Review of his observation charts showed that there had been a clear deterioration in recorded observations, including hypotension for the two preceeding hours. However, the Early Warning Score had been calculated incorrectly, and no escalation had occurred.

What evidence is there that rapid response systems are effective in preventing patient deterioration and improving outcomes?

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Invasive Streptococcal A Infections and Intravenous Immunoglobulin

Invasive Streptococcal A Infections and Intravenous Immunoglobulin

A middle aged woman presented with a one day history of swollen, painful red thigh after a prodromal sore throat. She had a exquisitely tender left thigh and knee with cellulitis. She was apyrexial, with normal heart rate and blood pressure, but had a respiratory rate of 24. She had a neutrophilia (28), elevated CRP, hyperlactataemia (4.1) an acute kidney injury (creat 170) and a mild coagulopathy. She was given analgesia, broad spectrum antibiotics (including clindamycin) and underwent a CT thigh which showed muscle swelling in the anterior compartment with fluid tracking up to the hip. Knee aspirate showed large number of gram positive cocci, later confirmed as Streptococcus A. Two hours into her admission the inflammation was involving the groin. She underwent exploration and debridement in theatre, and was noradrenaline dependent postoperatively. She was commenced on intravenous immunoglobulin on the same day. She required further debridement of the leg and lower abdomen on day 3. She gradually weaned off support, and underwent several more operations for closure of wounds and reconstructive surgery.

What is the role of IVIG in Invasive Streptococcal Infections

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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?

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Nutrition in Acute Pancreatitis

Nutrition in Acute Pancreatitis

A 55-year-old previously healthy lady was admitted with pancreatitis secondary to gallstones. Her admission modified Glasgow Score was 4, and CT scan showed approximately 70% necrosis of the pancreas encompassing the neck, body and tail with sparing of the head. She rapidly developed ARDS, AKI and vasoplegia, and subsequently developed abdominal compartment syndrome requiring decompressive laparotomy. Her later complications included intraabdominal collections requiring percutaneous drainage, upper GI bleeding, and staged closure of her laparostomy. She was initially commenced on enteral NG feeding but developed high NG aspirates despite pro-kinetics. Parenteral nutrition (PN) was commenced in combination with a ‘trophic’ enteral feed. Four weeks into her admission her triglyceride level was found to be elevated, necessitating lipid free PN and cessation of propofol. This led to a drop in her triglyceride level.

How should we manage the provision of nutrition in acute pancreatitis?

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Decompressive Laparotomy in Abdominal Compartment Syndrome

Decompressive Laparotomy in Abdominal Compartment Syndrome

A 55 yr old man developed severe necrotizing pancreatitis with multiorgan failure. One week into his illness he had developed multiple intra-abdominal collections and had high intra-abdominal pressures. Initial conservative management failed, percutaneous drainage of his collections failed to reduce the abdominal pressures, and he underwent decompressive laparotomy.

What is the evidence behind the current guidelines for the measurement of intra-abdominal hypertension and the use of decompressive laparotomy in the management of Abdominal Compartment Syndrome?Read More »