Management of Inhalational Injury

A 30-year-old man with no significant past medical history was admitted to ED from a house fire started by a piece of faulty electrical equipment. There were superficial skin burns only but some evidence of a possible inhalation injury with singed nasal hairs and a hoarse voice. Coughing resulted in expectoration of carbonaceous sputum with some haemoptysis. Arterial blood gas analysis revealed a PaO2 of 10.4 kPa on 40% oxygen a carboxyhaemoglobin level of 18%.

Semi-elective endotracheal intubation was performed using an uncut orotracheal tube. Ventilatory parameters were adjusted to give a tidal volume of 6-8 ml/kg and plateau pressure of less than 30 cmH20. Recruitment manouveres were performed to give an optimum compliance in the region of 40-50 ml/cmH20 with a positive end-expiratory pressure of 8 H20. The inspired fraction of oxygen was kept high (i.e. greater than 60%) until there was a fall of the carboxyhaemoglobin level to less than 5% at which point downwards titration was performed as guided by a target SpO2 of 94%.

Fibreoptic bronchoscopy was performed approximately six hours after admission to intensive care which demonstrated carbonaceous colonisation of the lower respiratory tract and areas of erythematous and denuded epithelium. Within 12 hours of intubation significant oedema of the face and upper airway had developed. A restrictive fluid regimen was instituted and there was gradual resolution of this swelling over the next 3 days. At this time, gas exchange was satisfactory and the patient was successfully extubated before being discharged to the high-dependency unit.

How is inhalational injury managed on the ICU?Read More »

Pneumococcal Sepsis

An elderly man with a background of ischaemic heart disease, severe aortic stenosis and type 2 diabetes mellitus presented following recent travel from Hong Kong with shortness of breath and hypoxia. A chest X-ray confirmed left lower lobe consolidation (CRP 502, WCC 22) and he was commenced on broad spectrum antibiotics (Tazocin and Clarithromycin). Over the following 12 hours he deteriorated on the ward, with worsening hypoxia, hypotension and anuria.

He required emergency admission to intensive care for intubation and ventilation, and required inotropic support. He developed a severe metabolic acidosis and rising lactate, for which  haemofiltration was commenced. Vasopressin was added, followed by dobutamine, and hydrocortisone started for inotrope resistant hypotension. He remained ventilated on 100% oxygen, with high pressure support. He had a positive pneumococcal antigen, and high dose benzylpenicillin was added to his antibiotic regime, along with Oseltamivir (Tamiflu). Despite 12 hours of intensive therapy his acidosis worsened and he failed to respond to increasing doses of inotropic support, dying 30 hours after presentation to hospital.

What are the clinical features of pneumococcal sepsis?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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Thrombolysis in Pulmonary Embolism

An elderly female was admitted under the care of the orthopaedic team with a 2 week history of decreased mobility due to right knee pain. She had a past medical history of chronic atrial fibrillation, treated with amiodarone, and asthma which was well controlled on salbutamol inhalers. She was not on warfarin. Bony injury was ruled out clinically and radiologically and she was treated with simple analgesia. Whilst on the ward, she deteriorated acutely after complaining of shortness of breath. A cardiac arrest call was put out.

On arrival of the cardiac arrest team, she had a cardiac output. On examination, she was hypotensive (BP 70/50 mmHg) with a heart rate of 55 bpm. She was markedly cyanosed with a respiratory rate of 30 breaths per minute with oxygen saturation of 75% on high flow oxygen through a reservoir bag. Her Glasgow Coma Score was 7 (E1V2M4). There was no evidence of calf swelling or tenderness. Arterial blood gas analysis revealed marked type 1 respiratory failure – pH 7.2, pO2 5.4kPa, pCO2 7.8kPa, HCO3 19mmol/l and lactate 4mmol/l .

She was rapidly intubated, and resuscitated with a total of four litres of crystalloids and colloids. Invasive blood pressure monitoring was established. A clinical diagnosis of acute pulmonary embolus was made. She remained unstable despite resuscitation, requiring frequent boluses of vasopressors and adrenaline thus being too unstable to be transferred for a CT pulmonary angiogram. A bedside echocardiogram showed a markedly dilated right heart with elevated right heart pressures. There was paradoxical movement of the interventricular septum. Left ventricular function was also slightly impaired.

It was decided to thrombolyse the patient. As alteplase was being readied, the patient arrested. The initial rhythm was pulseless electrical activity with a rate of 40 beats per minute. She was resuscitated as per Advanced Life Support (ALS) guidelines and received adrenaline and atropine intravenously. After two cycles of cardio-pulmonary resuscitation (CPR) and the administration of thrombolysis, she regained cardiac output but remained hypotensive and hypoxic. An adrenaline infusion was commenced through a peripheral line. Despite this, she arrested six further times with increasing inotropic support requirement. After two hours from the initial cardiac arrest call, the decision was made to stop resuscitation.

Post-mortem results confirmed the presence of a large pulmonary embolus as well as bilateral deep venous thromboses (DVTs).

What is the evidence for the use of thrombolysis in pulmonary embolism?Read More »

Metformin Associated Lactic Acidosis

Metformin Associated Lactic Acidosis

A 65-year-old female, presented with epigastric pain and a 3-day history of diarrhoea and vomiting, dry mouth and breathlessness. She had also experienced a transient loss of vision three days earlier. Her past medical history included type 2 Diabetes, hypertension (on ramipril), hypothyroidism. On arrival, her GCS was 15/15. She was tachypnoeic (respiratory rate 31 breaths/minute) but maintained oxygen saturations at 98% on high-flow oxygen. On auscultation, she had bibasal crepitations.  She was tachycardic (irregularly irregular pulse of 130 beats/minute), had cool peripheries and dry mucous membranes. Her BP was 105/39mmHg. She had tenderness in her lower abdomen. Her initial arterial blood gas revealed a marked metabolic acidosis (pH <6.8, pO2 23.1, pCO2 1.9) with unrecordable bicarbonate and lactate levels. She was referred to the surgical and critical care teams with a working diagnosis of ischaemic bowel secondary to an embolic phenomenon (atrial fibrillation and possible amaurosis fugax).

She was resuscitated in ED with 4 litres of crystalloid but rapidly deteriorated, requiring vasopressor support to maintain her blood pressure. Her metabolic disturbance did not not correct with resuscitation and her lactate now registered as >15. Bloods showed Na 140, K+ 6.3, urea 35, Cr 1105. A decision to intubate was made in view of a deteriorating conscious level and need for urgent filtration and invasive monitoring. Noradrenaline (0.3mcg/kg/min) and dobutamine (26mcg/kg/min) were required to achieve a satisfactory blood pressure and she was commenced on CVVHDF. She was considered to unstable for transfer to CT or an emergency laparotomy. Her metabolic disturbance remained severe (pH<6.8 and lactate 13.9).

Within 24 hours her metabolic state had improved (pH 7.19, pO2 7.19, PCO2 2.5, HCO3 10, BE -28.1, Lac 6.7) and she became more cardiovascular stability. A CT effectively excluded an intra-abdominal catastrophe. Renal failure secondary to dehydration complicated by Metformin Associated Lactic Acidosis (MALA) appeared to be the most likely presentation. Her condition continue to stabilise and her vasopressor support and RRT was weaned over the next 7-10 days

What are the risk factors, clinical features and management of metformin associated lactic acidosis?Read More »

Steroids in Cervical Spine Injury

Steroids in Cervical Spine Injury

A previously fit and well 46 year-old was admitted via the emergency department having sustained a neck injury whilst horse riding. She was unable to move her arms and legs immediately after the fall. On arrival to the Emergency Department, she was alert and orientated. Examination of the cardiovascular and respiratory system was unremarkable although there was evidence of diaphragmatic breathing.

Examination of her neurological system revealed:

•A sensory level at C6
•Absent upper limb reflexes except for brisk bicep reflex bilaterally
•⅖ power in shoulder abductors bilaterally
•Flaccid paralysis of her lower limbs
•No anal tone

She was initially managed in a hard neck collar with full spinal immobilisation. CT brain was reported to be normal. CT neck showed an obviously displaced fracture of C5 and C6 vertebral bodies. She was transferred to the intensive care unit for cardiovascular, respiratory and neurological monitoring while a definitive treatment plan was being considered. After discussions with the orthopaedic surgeons, it was decided not to commence high-dose steroids. This decision was reinforced after discussion with the local neurosurgical and spinal units. It was also decided not to surgically stabilise the c-spine due to the higher risk of respiratory complications. She was transferred to the spinal rehabilitation unit after 2 days.

What is the role of steroids in cervical spine injury?Read More »

Ethylene Glycol Poisoning

Ethylene Glycol Poisoning

A 50 year old man was found by the roadside by paramedics with a GCS of 13. On arrival he had a patent airway, but a GCS of 5 (E1 M3 V1). He had an elevated respiratory rate (30/min) and a profound metabolic acidosis (pH 6.97 pO2 16.8 pCO2 1.68 HCO3 2.8 BXS -30.8 COHb 0). The lactate was too high to be measured by the blood gas analyser and there was an elevated anion gap [(147+5.5) – (2.8+ 109) = 40.7] He was cardiovascularly stable with warm peripheries. His ECG revealed a prolonged QTc. He was intubated and 8.4% sodium bicarbonate was administered. His initial laboratory bloods showed CRP 11, white cell count 29.5 CK 2539 creatinine 213. Ethanol levels were <10 and Paracetamol and salicylate levels were within normal limits. He was given a dose of intravenous cefotaxime and his urine was sent for organic acids screening which revealed an enormous peak of glycolic acid and small increase in oxalic acid, consistent with an overdose of ethylene glycol.

After arrival in intensive care, the sodium bicarbonate had improved the pH to 7.2, with a residual lactaemia (15 as measured in the laboratory, without any interference from glycolic acid). CVVHDF was commenced. In order to inhibit futher metabolism of the ethylene glycol, 10% ethanol was commenced until fomepizole was available (an initial bolus of 800ml, followed by an infusion at 180ml/hr). Ethanol levels were monitored. Fomepizole was administered later that day abd the ethanol stopped (15mg/kg loading and 1mg/kg/hr). The renal function deteriorated despite CVVHDF (peaked at urea 28, creatinine 724 on day 4), which was continued for 5 days. Treatment for aspiration pneumonia was started in day 1 and cardiovascular support was continued (noradrenaline). Intermittent boluses of glycopyrolate were required to treat the bradycardia associated with fomepizole. A gradual improvement occurred and he had made a full neurological recovery within 2 weeks, with much improved renal function. He later admitted to drinking 250ml of antifreeze.

What are the clinical features and management of ethylene glycol poisoning?Read More »

Scoring Systems for Acute Hepatic Dysfunction

Scoring Systems for Acute Hepatic Dysfunction

A 40 year old was admitted to hospital with his first presentation of alcoholic liver disease with symptoms of jaundice (bilirubin 248), poor mobility, hallucinations and passing of black stool. On admission to hospital, he was lethargic with features of Grade II encephalopathy, was coagulopathic (INR 3.1), had deranged electrolytes (sodium 114, potassium 2.9), but a normal creatinine (54) and a raised white cell count (15.9). He was haemodynamically stable and had a haemoglobin of 119g/L with no signs of active bleeding. His abdomen was distended (ascites), he was visibly jaundiced and had spider naevi on his chest. An abdominal ultrasound was performed that showed liver cirrhosis, borderline splenomegaly, small volume ascites and normal kidneys. A full liver screen revealed no infective cause and his AST:ALT ratio suggested alcoholic liver disease. His prognostic indicator scores were all suggestive of severe alcoholic liver hepatitis (Maddrey score: 131; Childs: C; Lille Score: 1; GAHS: 10; MELD: 29). His serum ammonia level was 170. He was commenced on terlipressin, prednisolone and pentoxyphylline and thiamine. Despite this, his encephalopathy progressed to grade 4 and he required intubation and ventilation for airway protection and a presumed aspiration pneumonia. His liver function and coagulopathy continued to worsen, and he developed an acute kidney injury necessitating commencement of renal replacement therapy. He required noradrenaline to support his blood pressure. Ascitic tap ruled out spontaneous bacterial peritonitis. He was discussed with regional liver centres, but was not felt to be a transplant candidate. His liver and renal function continued to deteriorate and eventually treatment was withdrawn nearly 3 weeks into his admission.

Describe the scoring systems for assessing the severity of acute hepatic dysfunction.

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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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Lactate Physiology and Predicting Disease Severity

Lactate Physiology and Predicting Disease Severity

A middle aged man presented with urosepsis after several days antibiotic therapy in the community. He was in septic shock, with tachypnoea, tachycardia and hypotension. He had raised inflammatory markers and acute kidney injury. His initial lactate level was 14mmol/L with a significant metabolic acidosis (base deficit 21). He was commenced on iv antibiotics, noradrenaline and renal replacement therapy. Lactate levels cleared to less than 2mmol/L over the next 24hrs. He weaned off noradrenaline in 72 hours and CVVHDF over the next 5 days.

How is lactate produced and what is its significance in predicting the severity of critical illness?

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