Category: Domain 2

Diagnosis, Assessment, Investigation, Monitoring and Data Interpretation

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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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 »

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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Intra-Aortic Balloon Pump for Cardiogenic Shock

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A previously healthy 58-year-old male was admitted to hospital following an OOH cardiac arrest. The initial cardiac rhythm was VF. He remained on the ‘shockable’ side of the ALS algorithm and was managed accordingly with defibrillation and intravenous adrenaline.  ROSC occurred after 28 minutes. A 12-lead ECG showed a STEMI in the antero-septal territories.

Coronary angiography showed a proximal occlusion of the left anterior descending artery through which a drug eluting stent was inserted. Despite this and adrenaline (10-20mcg) boluses, the patient remained persistently acidotic and hypotensive. A diagnosis of cardiogenic shock was made and an intra-aortic balloon pump (IABP) was inserted via the left common femoral artery with subsequent improvement in haemodynamic parameters. The patient was transferred to a cardiothoracic critical care.

Transthoracic echocardiography showed a globally hypokinetic left ventricle (LV) with an ejection fraction (EF) of approximately 20%. Within the first 6 hours, he developed runs of non-sustained VT and frequent ventricular ectopics, which interfered with IABP triggering causing worsening haemodynamic instability. Triggering was switched from ECG to arterial pressure. Electrolytes were supplemented and intravenous amiodarone was commenced to manage the dysrhythmias. Targeted temperature management to 36 degrees Celsius for 24 hours was initiated. Anticoagulation for IABP was commenced and peripheral pulses were regularly monitored.

His dysrhythmias resolved with subsequent improvement of IABP performance. On day 3, the IABP was weaned to 1:2 ratio for approximately 6 hours and removed. A tracheostomy was inserted on day 7 and the patient underwent long term respiratory wean and neurological rehabilitation.

Describe the indications, contraindications, complications and basic principles of intra-aortic balloon counterpulsation balloon pump.Read More »

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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Echocardiography on ICU

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A 50 year old female presented with acute kidney injury and sepsis.  She required fluid resuscitation, haemofiltration and cardiovascular support for 2 days, following which she was discharged to the renal ward for on-going haemodialysis. She underwent dialysis every 2-3 days for the next 3 weeks. Whilst on the ward she deteriorated acutely one evening, developing respiratory distress, followed by a respiratory arrest. She was intubated and ventilated transferred to the critical care unit.

A CTPA was negative for pulmonary embolus, but showed large bilateral pleural effusions. Tracheal suctioning was initially clear but later copious blood stained secretions were removed. A bedside cardiac echo performed by the consultant intensivist showed a globally sluggish left ventricle, which was overfilled, and the inferior vena cava measured 3cm also suggesting fluid overload. A trial of furosemide failed and she was aggressively haemofiltered to remove the excess fluid. Troponin was only mildly raised, and not thought to be suggestive of an acute cardiac event. She was extubated 24 hours later, but had two further episodes of flash pulmonary oedema requiring non-invasive ventilatory support whilst haemofiltration was re-commenced for fluid balance reasons. In total twelve litres of fluid were removed, with significant improvement in the patient’s condition. Repeat echocardiography prior to discharge showed an improving left ventricular function and IVC measurement of 2cm with greatly increased compliance.

What is the evidence that focussed echocardiography helps guide decision-making in intensive care?Read More »

Acute Mitral Valve Failure

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An elderly woman woke from sleep with acute breathlessness and wheeze. She had been treated for late-onset asthma by her GP. She had no other previous medical history and was exceptionally active. In the emergency department she received standard treatment for acute severe asthma . A systolic murmur was noted and an echocardiogram requested. After 24 hours of relative stability she experienced a sudden deterioration in her breathing and despite increased therapy for her asthma she had a respiratory arrest.

Following resuscitation and emergency tracheal intubation she was transferred to the ICU. On examination she was peripherally cool. Chest auscultation revealed extensive wheeze and crackles. Investigations revealed a raised troponin I (0.92 ug/L) and raised BNP (530 pmol/L). Her CXR revealed pulmonary oedema and her ECG showed sinus rhythm without overt evidence of ischaemia.

Initial problems included poor oxygenation, oliguria and a low cardiac output state (LiDCO revealed cardiac index of 2.1 l/min/m2). She received norepinephrine (up to 0.6 mcg/kg/min) and dobutamine (up to 40 mcg/kg/min). Levosimendan was introduced to augment her cardiac function as her CI had not achieved to 2.5l/min/m2. Norepinephrine was increased to maintain a MAP over 65mmHg. After levosimendan her urine output, acid-base status and CI were not substantially improved. The dobutamine had been stopped and she remained on norepinephrine.

An echocardiogram revealed hyperdynamic LV and RV and mitral regurgitation, which was initially assessed as being moderate in severity. Cardiac surgical opinion was that the risk of mitral valve surgery was unacceptably high.

Over the following few days she had problems with recurrent compromising atrial fibrillation and was treated with varying degrees of success with a variety of measures including DC cardioversion, amiodarone, metoprolol, digoxin and verapamil. Diuresis was obtained with a frusemide infusion and ramipril was introduced. Her CXR appearances improved and ventilation became easier.

On the 3rd day a trans-oesphageal echocardiogram confirmed severe mitral regurgitation (MR) with prolapse of the posterior mitral valve (MV) leaflet due to a ruptured chordae tendinae. There was resultant left atrial enlargement and pulmonary hypertension with an estimated PA systolic pressure of 60-70mmHg. Within a week she was weaned from ventilatory support and recovered sufficiently to mobilise independently prior to discharge home.Read More »

Refractory Status Epilepticus

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A middle aged man presented with seizures. For 4 days he had been feeling unwell with coryzal symptoms, frontal headache and dizziness. He had ‘not been himself’ for some months. He had no previous medical history and had never had a seizure before. The ambulance crew noted that he was confused and witnessed a generalised tonic-clonic seizure. On arrival in hospital he was severely agitated and uncooperative and received IV lorazepam.

He was not adequately protecting his airway, saturations were 100% on high flow oxygen, temperature was 37.8, his pulse was 88, BP 129/90mmHg, blood sugar was 7.7. Clinical examination did not reveal any abnormality except for diminished level of consciousness. A presumptive diagnosis of meningitis / encephalitis was made. His trachea was intubated, he received fluids, parenteral vitamins, IV ceftriaxone and acyclovir. A CT head (with contrast) was obtained and a lumbar puncture were normal. His blood tests, CXR, urinary toxicology screen, and ECG were non-contributory. Arterial blood gas analysis revealed changes consistent with being post ictal and then (whilst ventilated) normalised.

His sedation was weaned and once extubated he remained very drowsy, even 18 hours after his last sedation. A Glasgow Coma Score (GCS) was recorded at E1V1M5 (7/15). His pupils were equal and reactive, and he was moving all 4 limbs. Both plantar responses were down-going, and tone and reflexes were symmetrical. He had myoclonic jerking of his left hand but no rhythmical muscle activity was evident. To protect his airway he required reintubation of his trachea and re-institution of ventilation.

In addition to sedation with propofol and alfentanil he received therapeutic phenytoin. An electroencephalogram (EEG) performed on his second day, off sedation, revealed continuous periodic sharp and slow wave complexes at around 1Hz with intermittent high amplitude waves in the left temporal region and bursts of rhythmical activity in the right temporal region. At the time of the EEG he had some abnormal motor activity – continuous movement of his fingers and twitching of an eyelid and rhythmical jerking of both of his arms. An MRI of his brain was normal.

In this clinical context the EEG was interpreted as being consistent with encephalitis and non-convulsive status epilepticus.  Phenobarbitone was started in addition to the phenytoin. Normothermia and normoglycemia was maintained. To improve the management of his non convulsive status we continuously monitored his cerebral electrical activity with a bispectral index (BIS) monitor and bitemporal EEGs. We targeted a burst suppression of 20-50%. Propofol was ineffective at reducing the BIS without causing limiting hypotension but midazolam was effective.

Further investigations did not further our search for the primary diagnosis. A further EEG was performed 24 hours later, off midazolam but whilst on 350mg/hr of propofol. He developed some rhythmical motor activity and his EEG revealed ongoing abnormal electric activity, consistent with continued non-convulsive status, which resolved in response to a bolus of propofol. A possible diagnosis of limbic encephalitis was considered and methylprednisolone (1g IV) was administered.

A repeat MRI showed increased abnormal signal changes in the amygdala and hippocampus, which is supportive of the diagnosis of limbic encephalitis.

Despite optimal medical treatment his EEG showed more severe and continued abnormal electrical activity. Thiopentone was added to his anti-seizure regime. By the 19th day from initial presentation multiorgan failure had developed. He required ventilation with high airway pressures and high inspired oxygen concentrations for lung injury due to ventilator associated pneumonia, vasoactive drugs to support his cardiovascular system through the associated sepsis, haemofiltration for renal failure and had ileus with failure of enteral feeding. There were still signs of seizure activity despite concurrent administration of propofol, midazolam, phenytoin, levetiracetam, phenobarbitone and sodium valproate. Supportive treatment was withdrawn following diagnosis of brain-stem death. His family did not permit a post mortem examination.Read More »

Management of Inhalational Injury

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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 »