Tag: Craig Walker

ICP Monitoring and Acute Liver Failure

ICP Monitoring and Acute Liver Failure

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A 28-year-old lady presented to the medical team jaundiced with cramping upper abdominal pain and multiple episodes of vomiting over the previous day. She admitted ingesting Paracetamol 8 grams 3 days previously (staggered throughout the day) ostensibly to treat a frontal headache. She had been commenced on Citalopram 1 week previously for depression but denied taking any intentional overdose. On examination, she was slightly drowsy but GCS 15. HR 109, BP 136/92. Sats 98%on air. Her chest was clear, she was warm peripherally but jaundiced with some epigastric and RUQ tenderness on palpation. Her urine output was 10-20ml/hr.

Full Blood Count revealed Hb 152, WCC 24.7, Plats 301. She was in acute liver failure with Bil 189, AST 22970, ALT 13040, ALP 426 and coagulopathic with PT 82, APTT 72, Fib 0.7 Urea 5.7, Cr 193. Paracetamol and Salicylate were not detected. She was not acidotic with H+ 35, OCI2 3.7, pO2 17, Bic 20, BE –3. Lactate 7.1.

She was commenced on N-acetylcysteine and transferred to Critical Care. She was reviewed by the Hepatobiliary surgical team and placed on the super-urgent list for liver transplant. 

On Day 2, she became encephalopathic with GCS E3M5V5 and she was intubated and ventilated.Her PT had increased to 168 (INR >15) and she became anuric. She commenced FFP and Cryoprecipitate transfusions that improved her PT to 17, APTT 34 and Fibrinogen 1.5. An Intracranial Pressure (ICP) monitor was inserted and an opening pressure of 19mmHg was found. 2 hours post-insertion, it was noticed that her right pupil had increased in size from 2mm to 4mm and was poorly reactive. ICP remained at 16 and pCO2 4.1.

A brain CT showed a large haematoma in the right frontal region around the ICP bolt (which was not in the brain parenchyma but sitting in the skull) and mass effect with 5mm midline shift. There was also some lack of grey-white matter differentiation and sulcal effacement in keeping with diffuse oedema and mass effect.

INR was 1.7 and so further FFP was given. She was discussed with the neurosurgical registrar (in a separate hospital) who advised they would not drain at present but he would discuss with his Consultant and call back. 

Soon after, her right pupil increased to 8mm and the left to 7mm. Repeat CT brain showed slightly increased right frontal haematoma with 6mm midline shift and global oedematous cortical changes but no herniation. The ICP readings were thought to be inaccurate due to proximal placement and she was medically treated for raised ICP with hypertonic saline, mannitol and then therapeutic hypothermia. Despite this treatment, her pupils were fixed and dilated and so a thiopentone infusion was commenced.

The neurosurgeons advised that they would insert a further ICP monitor when INR <1.3 and so further FFP was given. An ICP bolt was inserted and the opening pressure was >120.

Discussions between the ICU, hepatobiliary and neurosurgical teams confirmed that she had a non-survivable injury and so this was discussed with her family. She was rewarmed, paralysis and then sedation were discontinued, brain stem death testing took place and she was extubated in the presence of her family. She died on Day 3 and was referred to the Coroner for further investigation.

What is the rationale for measuring ICP in acute liver failure?

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Major Haemorrhage and Recombinant Factor VIIa Concentrate

Major Haemorrhage and Recombinant Factor VIIa Concentrate

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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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Non-invasive Ventilation in Severe Community Acquired Pneumonia

Non-invasive Ventilation in Severe Community Acquired Pneumonia

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An elderly man attended the Emergency Department with a 3-day history of increasing breathlessness, a cough productive of white sputum and intermittent left anterior chest heaviness. He had no significant comorbidities, and lived independently. On examination, Sats were 80% on high flow face mask O2, RR was 20 and there were bilateral crepitations to both mid-zones. ABG showed type one respiratory failure with pO2 5.7 and Lactate 2.0.  CXR revealed left-sided consolidation and bilateral upper lobe venous diversion with small bibasal pleural effusions. HR was 75, BP 102/57 with an elevated JVP. Temperature was 38 with WCC 14.6.  An ECG showed sinus rhythm with inferior T wave inversion. Urea was 20 and Creatinine 105 (baseline 59). Troponin was 2.9 (normal range <0.05). The impression was of left-sided community-acquired pneumonia and acute renal impairment with Congestive Cardiac Failure (CCF) likely precipitated by a recent myocardial infarction. He was admitted to ICU, given broad-spectrum antibiotics and treatment for acute coronary syndrome and he was commenced on Non-Invasive Ventilation (NIV). He required FiO2 0.8 and PEEP 10 to maintain pO2 >8. Echocardiography showed at least moderate LV systolic impairment, moderate MR and Grade 3 diastolic dysfunction.  He was commenced on Noradrenaline and Dobutamine infusions. On day 2, he became profoundly bradycardic and had an asystolic cardiac arrest. Spontaneous circulation was restored following 1 minute of CPR and Adrenaline 1mg IV. He was intubated during the arrest. Despite ROSC, he continued to deteriorate with increasing pressor requirements and worsening AKI . After discussion with family, treatment was withdrawn.

What is the evidence for using non-invasive ventilation in patients with severe community acquired pneumonia?

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Invasive Streptococcal A Infections and Intravenous Immunoglobulin

Invasive Streptococcal A Infections and Intravenous Immunoglobulin

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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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Management of Life-Threatening Tricyclic Antidepressant Overdose

Management of Life-Threatening Tricyclic Antidepressant Overdose

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A 44-year-old lady was brought to ED by ambulance after her partner found her drowsy in her bedroom with multiple empty packets of Amitriptyline scattered around the bed. The ambulance crew found no other medications in the immediate vicinity. Her partner had last seen her two hours previously that evening and described a history of depression, previous overdoses and chronic alcohol excess.  On arrival in ED, her airway was self-maintained but she had signs of vomitus around her mouth and smelled strongly of alcohol. Heart rate was 125, NIBP 92/38 and ECG showed sinus rhythm with prolonged PR and QRS intervals (240ms and 200ms, respectively). ABG showed a metabolic acidosis with lack of respiratory compensation, with hyperlactataemia (4.1). GCS was 9 (E2M5V2) although she appeared agitated with bilaterally dilated pupils. There was no external evidence of injury. The impression was of life-threatening Tricyclic Antidepressant (TCA) overdose within the last 2 hours along with alcohol ingestion.

What are the main features of a Tricyclic Antidepressant overdose? What treatment options are available?

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