Category: Basic Sciences

Graft versus Host Disease

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A 34-year-old woman received a small bowel, pancreas and abdominal wall transplant.

Despite the operation being technically very difficult and prolonged, she initially recovered well after the procedure and her transplanted bowel started to work. However, after a few days she started developing respiratory complications eventually requiring re-intubation despite antibiotics. She went on to develop multi-organ dysfunction requiring vasopressor support and renal replacement therapy. Antifungals and co-trimoxazole were added, with no additional benefit noted.

A skin rash started to develop, which raised the suspicion of Graft versus Host Disease (GvHD). A diagnostic test was performed (chimerism of peripheral blood leucocytes), and it confirmed the diagnosis of GvHD.

Doses of immunosuppressants such as tacrolimus, mycophenolate mofetil were increased and steroids were started too.

An experimental therapy of mesenchymal stem cells infusion was also employed, but she continued to deteriorate further and she eventually died after a prolonged admission on ICU.

Graft versus Host Disease – what it is, how to diagnose it, how to treat itRead More »

Extracorporeal CO2 removal

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A 42 year old man presented with a week-long history of increasing shortness of breath, cough  (productive of purulent sputum) and fevers on a background of significant chronic lung disease. He had a ten year history of interstitial lung disease and was on the waiting list for a lung transplant. He used oxygen at a rate of 2 litres per minute at home, 24 hours a day. His usual exercise tolerance of 200 metres had been significantly reduced for the past week. His regular medications included seretide and salbutamol inhalers, lansoprazole, azathioprine, prednisolone alendronate.

On arrival in hospital, he was alert and orientated. He had a patent airway, but was tachypnoeic (rate of 50/minute) using his respiratory accessory muscles and a tracheal tug was evident. An arterial blood gas revealed type two respiratory failure (pH 7.26; pO2 8.14, pCO2 7.52 on 15 liters/min of face mask oxygen). He was hypotensive (80/40mmHg) and tachycardic (130/minute, sinus rhythm). A pyrexia of 39.2°C was recorded. Blood results showed normal renal function, a slightly elevated white cell count of 14.

The patient was admitted to the high dependency for close monitoring in view of his history and presentation. He was commenced on treatment for a presumed infection (viral or bacterial) with oseltamivir, co-amoxiclav and clarithromycin and given three “pulsed” doses (750mg) of methylprednisolone. He remained stable for the next twelve hours.

Early the next morning, he became very hypoxic (oxygen saturations less than 50%), bradycardic (<35 beats per minute) and had a brief hypoxic respiratory arrest. He received 1 cycle of cardiopulmonary resuscitation and was intubated. There was subsequently a return of spontaneous circulation.

The next 24 hours involved a period of difficulty with ventilation. His peak airway pressures were very high, despite being paralysed and a low volume/high respiratory rate strategy being employed. He was discussed with a tertiary respiratory centre and it was decided that he should be transferred for insertion of a pumpless arteriovenous interventional lung assist (for extracorporeal carbon dioxide removal) as a bridge prior to lung transplantation. He had formal ultrasound measurement of his femoral arteries. His left common femoral artery was widely patent (AP and transverse diameter of 8-9mm throughout), but the right was only 4-5mm throughout.

In the meantime, his peak airway pressures were consistently between 35 and 40cmH2O, despite tidal volumes of 230ml, 3.8ml/kg). With a rate of 32-35 breaths per minute, his pH was  initially maintained above 7.2, with a pCO2 of 9-11kPa. Over the course of the next few hours, this became increasingly difficult to achieve. His oxygen requirements did not escalate (an FiO2 of 0.6 provided a pO2 of 8-9kPa). When his pCO2 increased to 15.4kPa and his pH dropped to 7.17, further adjustments were made and the PEEP decreased to 5cmH2O from 10cmH2O. His noradrenaline requirements were increasing and with the aid of the cardiac output monitoring, he was cautiously given fluid with a good response.

He was transferred to the centre in which a lung transplant could be performed within hours of the referral. A Novalung device was inserted and he underwent a bilateral lobar lung transplant several days later. He was in hospital for 6 weeks and made a very good long-term recovery. At six months, he was extremely well and was undertaking his activities of daily living completely normally with stable lung function. He even managed to complete an eight mile bike ride.

What is the rationale for extracorporeal lung assist?
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Faecal Peritonitis: The Role of Laparostomy

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A 68-year-old previously fit woman was admitted with left lower abdominal pain and signs of cardiovascular shock. She had had a 2 day history of crampy left lower abdominal pain and altered bowel habit. Clinically she had a diagnosis of bowel perforation with generalised peritonitis. She was exhibiting signs of shock with a pronounced tachycardia and a reduced systolic blood pressure.

She was started on fluid resuscitation and intravenous antibiotics. After her cardiovascular system stabilised she was taken to the operating theatre where she had a laparotomy. A sigmoid perforation was found with four quadrant faecal contamination. A Hartmann’s procedure was performed. A laparostomy was decided upon at the first instance, and was covered with a VAC dressing.

She was transferred to the intensive care unit (ICU) still intubated and ventilated.

Her condition rapidly worsened on the ICU. She required vasopressor support intra-operatively and her requirements rapidly escalated. She seemed to stabilse over the next 36 hours. Her condition then worsened and she was taken back to theatre for a washout of her peritoneal cavity. A number of collections were found and further soiling of her abdomen was evident. Her condition remained the same for the next 12 hours but then started to show an improvement again. She continued to make a good response to treatment over the next 3-4 days. She had another washout at 4 days. She was extubated on day 5 and invasive monitoring and cardiovascular support was no longer needed.

 

What is the role of laparotomy in the management of faecal peritonitis?Read More »

Thrombotic Thrombocytopaenic Purpura

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A previously fit and well 64 year old gentleman presented to the acute medical unit with a two-week history of lethargy, bruising, dark urine and an episode of transient facial numbness, blurred vision and dysarthria lasting 30 minutes. Clinical examination revealed mild jaundice, multiple bruises and a palpable liver edge but was otherwise normal. His respiratory rate was 14 breaths/minute with normal oxygen saturations. He was in sinus rhythm with a pulse of 68 beats/minute and non-invasive blood pressure was 130/70. He was GCS 15 and was apyrexial.

His full blood count revealed a haemoglobin of 94 g/L, platelets 9 x109/L, and white cell count 9 x109/L. A blood film showed red cell fragmentation, spherocytes, polychromasia, poikilocytosis and no platelet clumps. Reticulocytes and lactate dehydrogenase were raised at 168.6 x 109/L and 3027 iu/L respectively. Liver function tests revealed a bilirubin of 49 µmol/L but were otherwise normal. A liver ultrasound showed fatty infiltration. Clotting was normal and direct antiglobulin test negative. Urea and electrolytes were normal, creatinine 80 µmol/L and the C reactive protein was 37. ADAMTS13 assay showed complete absence of activity. CT brain was normal.

He was reviewed by the haematologists who diagnosed thrombotic thrombocytopenic purpura and referred him to the intensive care unit for plasma exchange. He received a three-day course of methylprednisolone, was intubated due to agitation, received plasma exchange with octaplas replacement that increased from 2 litre to 5 litre exchanges, and rituximab 750mg.

He deteriorated progressively with: vomiting, anaemia requiring blood transfusions, worsening thrombocytopenia, acute kidney injury with a peak creatinine of 457 µmol/L, an inferior ST elevation myocardial infarction, and a posterior cerebral artery territory infarct.

On day 5 he developed fixed and dilated pupils. Mannitol 1g/kg was administered and an urgent CT brain performed. This revealed multiple infarcts in both cerebral hemispheres and right cerebellum, loss of grey-white differentiation, 5mm midline shift and low cerebellar tonsils.

After discussion with the neurosurgeons it was decided this was an unrecoverable injury. In agreement with his family, end of life care was instituted and he died within 24 hours.

Describe the management of Thrombotic Thrombocytopaenic Purpura.Read More »

Dexmedetomidine Sedation and Delirium

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A 35-year-old man was admitted through the Emergency Department with a three-day history of sore throat, drooling of saliva and fever. In the twenty-four hours leading up to his admission he had reported increasing difficulty breathing and hoarseness. His past medical history included obesity and non-insulin dependent diabetes mellitus.

On initial assessment he was found to be stridulous, drooling, tachypnoeic, tachycardic and febrile. Supplemental oxygen was applied and intravenous access obtained, with blood cultures being sent prior to administration of broad-spectrum antibiotics (Ceftriaxone, Benzylpenicillin and Metronidazole). Despite nebulised Adrenaline, intravenous fluid and intravenous dexamethasone, he continued to deteriorate and was transferred to the anaesthetic room for definitive airway management. Findings at intubation were consistent with acute epiglottitis. Swabs were taken and oral fibreoptic intubation was successfully performed.

Following admission to the ICU, he was mechanically ventilated and sedated with infusions of Propofol and Remifentanil. Antibiotic therapy was continued and he was commenced on regular dexamethasone to reduce epiglottic oedema. He required a low- dose noradrenaline infusion to maintain blood pressure, and was commenced on an insulin sliding scale. Two days after admission his airway was reassessed with direct laryngoscopy, and was found to be significantly less oedematous.

At this stage a sedation hold was performed, with the patient opening eyes spontaneously and seeming to obey commands. He was extubated to humidified facemask oxygen but shortly afterwards became agitated, combative and delirious (CAM-ICU positive). The patient was re-intubated within a two-hour period and Propofol and Remifentanil sedation was recommenced. Over the following two days, he remained inappropriate on daily sedation holds, and by this stage was receiving bolus doses of Haloperidol for episodes of acute agitation. CT imaging of his brain revealed no abnormality, and lumbar puncture was negative for central nervous system infection. Intravenous dexamethasone had been weaned, in view of the improvement in epiglotittis seen at laryngoscopy.

By day six of his admission he remained neurologically inappropriate on sedation hold, and was changed to an intravenous infusion of Dexmedetomidine at 0.7 mcg/kg/hr. Remifentanil was weaned off at this time, and Propofol infusion was reduced to baseline levels. This continued for a further twenty-four hours, by which time he was neurologically appropriate on sedation hold, obeying commands, and was extubated uneventfully.

On direct questioning, the patient did not recall his first extubation episode on Intensive Care. He did recall a combination of vivid visual and auditory hallucations, including the presence of insects in his bed, hearing persecutory voices and a feeling of helplessness and fear. He made a full recovery, and these symptoms had fully resolved by the time he was discharged from hospital.

What is the role of dexmedetomidine in the prevention and management of ICU delirium?

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The Role of Capnography during Cardiac Arrest

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 A 68 year-old gentleman was admitted to the Emergency Department in cardiac arrest. He had complained of sudden onset upper abdominal pain to his wife immediately prior to a collapse, and bystander cardiopulmonary resuscitation (CPR) was commenced whilst emergency services were called. He had a background of ischaemic heart disease, insulin-dependent diabetes, peripheral vascular disease and hypertension.

On arrival, the Paramedic crew found him to be in ventricular fibrillation was the predominant rhythm. Despite appropriate advanced life support with defibrillation and administration of adrenaline and amiodarone over multiple cycles. His airway was supported with an I-Gel supraglottic airway device, and he was transferred to hospital urgently.

Ischaemic heart disease is the leading cause of death in the world, and sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease. Early and effective CPR, early defibrillation and physiological support post-resuscitation form the chain of survival [1].

Assessment of the patient’s airway on arrival in the Emergency Department revealed evidence of vomit in the pharynx, and endotracheal intubation was performed. Vomitus was aspirated from his endotracheal tube, indicating pulmonary aspiration either at the time of collapse or during the resuscitation attempts. Sidestream capnography was connected to a self-inflating bag administering high-concentration oxygen. The initial capnography indicated a flattened end tidal carbon dioxide (EtCO2) trace with a highest partial pressure of 1.5 kPa. Chest auscultation was performed and air entry was confirmed as being equal bilaterally.

Chest compressions continued uninterrupted and by this stage the overall resuscitation attempt had been ongoing for 45 minutes. The rhythm had changed to pulseless electrical activity, and despite effective CPR, administration of adrenaline and fluids, there was no return of spontaneous circulation (ROSC). Blood gas analysis revealed a severe metabolic acidosis (pH 6.8, lactate 15.2 mmol/L) and by this stage the highest EtCO2 recorded was 0.9 kPa. Following discussion with the team, and on the grounds of futility, the resuscitation attempt was abandoned.

What is the role of capnography in cardiac arrest?

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The Role of Antibiotics in Acute Pancreatitis

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A 65-year-old woman was admitted with a two-day history of feeling non-specifically unwell, severe upper abdominal pain, anorexia and vomiting. On examination she was tachycardic, hypotensive with epigastric tenderness and guarding. Admission amylase was 1024 mmol/L. A diagnosis of acute pancreatitis was made and she was admitted for conservative management with IV fluids and analgaesia. Her initial Ranson score was 3 placing her at moderate risk of of death. Abdominal ultrasound scanning showed a swollen pancreas with a small amount of free fluid but no gallstones or obstruction to the biliary system. Over the next twelve hours she deteriorated on the ward, developing type 1 respiratory failure for which she was referred to intensive care.

On admission to ITU she was semi-electively intubated and ventilated. A low-dose infusion of noradrenaline required to achieve adequate mean arterial pressure. A CT scan showed inflammatory changes and free fluid around the pancreas with possible early pseudocyst formation but no necrotic areas. Two hours after admission she became pyrexial at 39.5°C with a modest increase in her noradrenaline requirements. Peripheral blood cultures were taken and empirical imipenem started following discussion with microbiology. Subsequent repeated microbiological cultures of blood, ascitic fluid, urine and sputum were negative. A nasojejunal tube was passed to allow enteral feeding.

Over the next 48 hours her sedation was weaned and her respiratory function improved. Vasculitis screens, viral serology, lipids, etc. were all negative or normal. Despite her clinical improvement she remained pyrexial with an elevated CRP and white cell count. Further microbiological sampling was unhelpful, serum procalcitonin middling and repeat CT scan showed maturation of her pseduocyst. Fine needle aspiration was performed and subsequently proved culture negative. Her imipenem was stopped after 7 days after gradual resolution of her noradrenaline requirements. Surgical tracheostomy was performed on day 11 to facilitate ventilatory weaning and she was discharged to the ward on day 21.

What is the role for antibiotics in acute pancreatitis?Read More »

Decompressive Craniotomy in Traumatic Brain Injury

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A 20 year-old man was admitted to his local district hospital with a severe head injury following an assault. On arrival in the Emergency Department he was agitated with a reduced conscious level, with evidence of blunt trauma to the head and neck. Prior to intubation, his Glasgow Coma Score (GCS) was recorded as 7 (E1V2M4), and with cervical spine precautions he underwent intubation with subsequent mechanical ventilation and sedation.

An urgent CT brain and cervical spine revealed early evidence of intracerebral contusions with diffuse areas of petechial intracerebral haemorrhage identified. Nasal and maxillary fractures were also seen, with no cervical spine pathology identified. He was transferred to the regional neurological centre for assessment and ongoing management.

On arrival in the Neurosurgical Intensive Care unit the patient underwent insertion of an intracranial pressure monitor revealing an intracranial pressure (ICP) of between 30-35 mmHg. Pupil reactivity was sluggish bilaterally. Sedation was changed to infusions of propofol, fentanyl and midazolam, positioning was optimised with 20 degree head-up tilt, endotracheal tube ties were replaced and targeted mechanical ventilation to EtCO2 4- 4.5kPa. Central venous access was established and an infusion of Noradrenaline was used to target cerebral perfusion pressure to 70mmHg.

Initial medical management stabilised ICP below 25mmHg, but within the next 12 hours this began to rise despite neuromuscular blockade and infusion of hypertonic saline. Further CT imaging revealed progression of the intracerebral contusions with developing oedema. The patient was transferred to the operating theatre for insertion of an external ventricular drain. CSF drainage resulted in an immediate but small improvement in ICP but again over the next 12 hours it began to rise, and decision was made for bifrontal decompressive craniectomy.

Subsequent recovery was slow and was complicated by ventilator-associated pneumonia, a protracted tracheostomy wean and severe agitation. The patient underwent intensive neuro-rehabilitation and had been decannulated, but was left with persistent cognitive impairment, seizures and depression.

What is the rationale for performing decompressive craniotomy in TBI?

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Sleep Deprivation on the ICU

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A 70-year-old lady was admitted to the Intensive Care Unit (ICU) with respiratory failure and septic shock secondary to pneumococcal pneumonia. She developed multi- organ failure, requiring a prolonged period of mechanical ventilation and weaning, and also developed acute kidney injury requiring haemofiltration. Once a tracheostomy was performed and sedative infusions weaned, she was noted to be acutely delirious. Her sleep pattern was severely disrupted, with extended periods of nighttime wakefulness and sleep fragmentation, increased daytime sleep and difficulty with sleep initiation requiring pharmacological intervention.

Following exclusion of organic causes including CT brain imaging, the delirium was managed with a combination of antipsychotic medications including haloperidol, mirtazapine and quetiapine. Benzodiazepine-based night sedation was used but found to be ineffective in establishing sustained sleep.

A trial of night sedation with infusion of Propofol did not have any ongoing or long-lasting benefit other than the immediate sedative effects and providing control of agitation. A trial of Dexmedetomidine infusion also yielded similar results, although a more sustained daytime anxiolytic effect was noted. Benzodiazepine therapy was changed to supplementation of Melatonin. At around this time, the delirium began to resolve and the patient was able to more actively engage in physiotherapy and patient care. By the time of ICU discharge over thirty days later, and following successful weaning and decannulation, the patient’s sleep pattern had improved significantly.

What are the implications of sleep deprivation in the critically ill patient and how can it be managed?

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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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