Category: Neuromuscular

Neurological and Neuromuscular

Adjunctive Therapies in Bacterial Meningitis

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A 42 year old female with type 2 diabetes presented to hospital with fevers, malaise and headache. She had become unwell 7 days earlier with coryzal symptoms, feverishness, and cough with green sputum. On examination she was unwell and intermittently drowsy but gas exchange was adequate and she was haemodynamically stable with lactate 1.5 units. Temperature was 39.6oC and glucose was 15.8 units. Chest x-ray showed bibasal consolidation. CRP was 35 units and white cell count was 12.9. She received ceftriaxone 2 g, clarithromycin 500 mg, intravenous crystalloid 1000 mL and an insulin sliding scale.

One hour after admission the patient deteriorated with GCS 6 and non-purposeful shaking movements of the right arm and leg, which resolved with diazepam 5 mg intravenously. Her airway became partially obstructed despite nasopharyngeal and oral airways and she was urgently intubated. Aciclovir 900 mg was given and the patient was transferred to the ICU.

CT head showed no abnormality. A lumbar puncture revealed turbid yellow-tinged cerebrospinal fluid (CSF). Dexamethasone 10 mg was given. A phenytoin infusion was started. Sedation was maintained with propofol and fentanyl.

The CSF showed Gram positive cocci and a white cell count of 1274 units with neutrophils 1248 units. CSF glucose was 0.3 units and protein was 5.5 g. Ceftriaxone twice daily and dexamethasone four times daily were continued and acyclovir was discontinued. Blood cultures and CSF both grew Streptococcus pneumoniae. Viral PCR was negative. After 48 hours the patient was extubated and then discharged to the ward without any neurological deficit. She went home 5 days after admission. Ceftriaxone was given for a total of 14 days, facilitated by the outpatient parenteral antibiotic therapy team. She was advised not to drive for 6 months.

What adjunctive therapies, if any, are effective in the treatment of bacterial meningitis?Read More »

Alpha-2 agonists for sedation

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A 66 year old woman was admitted to the ICU with acute type II respiratory failure secondary to a community acquired pneumonia (CURB-65 score 4) complicating severe COPD (FEV1 40% predicted). Collateral history revealed many concerning features; the patient had a poor exercise tolerance (mMRC dyspnoea scale score 3, exercise tolerance <100m), was alcohol dependent (drinking 120 units per week) and previously had been admitted to hospital with an exacerbation of COPD requiring NIV, and treatment for acute alcohol withdrawal.

 

Mechanical ventilation was commenced using a lung-protective strategy with permissive hypercapnia. Sedation was achieved using remifentanil and propofol, targeting a Richmond Agitation Scale Score (RASS) of -2 to 0. A noradrenaline infusion was commenced to maintain a mean arterial pressure of ≥65mmHg. A neutral cumulative fluid balance was targeted. Broad-spectrum antimicrobial therapy was continued as per local antimicrobial guidelines. Intravenous B vitamins were administered and enteral feeding was established via a nasogastric tube.

In view of the patient’s comparatively poor pre-morbid function and high risk of delirium, early extubation to NIV was identified as the preferred strategy. By day 3 the patient had improved such that this became a realistic goal. In order to prevent acute alcohol withdrawal, yet use benzodiazepines sparingly to avoid associated respiratory depression, remifentanil-propofol sedation was substituted for a clonidine infusion, which was continued following extubation. Low doses of chlordiazepoxide were used as rescue therapy in accordance with Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar) scoring.

The patient progressed well, was weaned from both NIV and clonidine and was discharged from HDU to a respiratory ward on day 8. She survived to hospital discharge.

 

What role do Alpha-2 Agonists have for sedation in critical care?Read More »

Post-operative Opioid-Induced Hyperalgesia

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An elderly female was admitted to the intensive care unit (ICU)following a planned hemi-hepatectomy to remove metastatic lesions from a previously resected primary colorectal cancer. The patient had declined neuraxial anaesthesia. The surgery proceeded uneventfully via a rooftop incision under general anaesthesia, which was maintained with remifentanil, sevofluorane and paralysis with atracurium.

30 minutes before the termination of the three hour operation, a bolus of 10mg of morphine was given intravenously and a patient-controlled analgesia (PCA) morphine pump was prepared. At emergence from anaesthesia, paralysis was reversed, and the patient was successfully extubated. In the ICU the patient was instructed in the use of the PCA. She was initially comfortable, but within 30 minutes she complained of worsening abdominal pain around the upper abdominal incision and became tachycardic.

To address this patient’s worsening post-operative abdominal pain 10mg of morphine was given intravenously. Simultaneously she was reassessed and the potential cause of the pain was sought. The abdomen remained soft and mildly tender. Drains were dry, and parameters including blood pressure, respiratory rate, haemoglobin, and arterial blood gases were satisfactory.

The morphine was ineffective. She was given 1g of intravenous paracetamol, a further bolus of 10mg of morphine and two sequential 500mL aliquots of crystalloid. Surgical review was requested. After another 20 minutes the pain had not diminished so she received a bolus of fentanyl and a trial dose of 100mg of intravenous tramadol. Unfortunately these measures did not reduce the pain at all. Although vital signs were unchanged, the patient was increasingly distressed.

There was no apparent clinical deterioration to account for the increased pain. Yet, control of her symptoms had clearly been lost and routine analgesia was ineffective. Urgent senior review was requested. Suspecting that she had become refractory to opioid analgesia, and concerned about the severity of the pain and its potential complications, the consultant stopped the patient’s PCA, increased the inspired oxygen fraction to 0.80 through a non-rebreathe mask, and gave 50mg of ketamine intravenously.

These interventions significantly improved symptoms over the next ten minutes. The patient remained conscious though slightly drowsy and her tachycardia settled. Simple analgesics and a low dose infusion of 2-5 mcg/kg/min (approximately 10-25 mg/h) of ketamine were prescribed. These effectively controlled her pain. After the patient had remained comfortable and clinically stable for several hours, the PCA was gradually re-introduced and the ketamine was discontinued. She was discharged to the ward the following day.

What is opioid-induced hyperalgesia?Read More »

Facilitation Of Donation After Circulatory Death

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A previously fit and well 45 year old man presented to the emergency department with a two-hour history of a sudden onset severe headache associated with weakness, vomiting and photophobia. He had a normal breathing pattern and oxygen saturations of 96% in air. He was hypertensive with a non-invasive blood pressure of 220/115mmHg and a pulse rate of 85 beats/minute in sinus rhythm. Neurological examination revealed a Glasgow Coma Scale (GCS) of 14/15 with a dense hemiparesis, with hemisensory neglect and dysarthria.

He deteriorated and dropped his GCS to 5/15. He was intubated and an urgent computed tomographic (CT) brain scan was performed that revealed a large right-sided intraparenchymal haemorrhage with 4mm of midline shift. Blood tests including full blood count, urea and electrolytes and clotting screen were normal.

He was discussed with the neurosurgeons who felt transfer to institute intracranial pressure monitoring or surgical intervention was not indicated. His blood pressure was managed with a labetalol infusion aiming for a target systolic blood pressure of ≤ 160mmHg. Seizure activity was managed with a 15mg/kg loading dose of phenytoin followed by a maintenance dose of 300mg once daily nasogastrically. Sodium levels were monitored closely and hypotonic fluids avoided.

By day 5 he was making spontaneous respiratory effort, and his pupils were equal and sluggishly reactive. His GCS remained 3/15. A repeat CT was performed on day 9 due to no improvement in his clinical condition and revealed extension of the intraparenchymal haemorrhage with 8mm midline shift, effacement of the ventricles and loss of sulcal definition. A discussion regarding end of life care was held with his family who raised the possibility of organ donation. In agreement with his family, end of life care was instituted and he became an organ donor after circulatory death was confirmed.

How can we facilitate Donation After Circulatory Death?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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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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Management of Refractory Intracranial Hypertension

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A young man with no significant past medical history was admitted to the Emergency Department following an assault. His Glasgow Coma Score on arrival was 8 with a motor score of 4 and there was evidence of an external head injury. Pupils were symmetrically reactive. He was intubated to facilitate further management. Both primary and secondary surveys were unremarkable apart from multiple contusions to the face and scalp. Multi-slice CT showed no intrabdominal or intrathoracic injury but significant intracranial pathology with subarachnoid and intraventricular blood and multiple, principally frontal contusions. No associated neuraxial fracture was seen.

Urgent neurosurgical opinion was sought which confirmed no immediate target for surgical intervention. The patient was transferred to the intensive care unit where appropriate monitoring was established including the insertion of a fibreoptic subdural intracranial pressure bolt. Initial intracranial pressure was measured at 18 mmHg. Sedation with propofol and alfentanil infusions was titrated to a RASS score of -3, ventilation adjusted to a PaO2 > 13 kPa and PaCO2 4.5-5.0 kPa as per the Brain Trauma Foundation guidelines and an infusion of noradrenaline started to achieve a cerebral perfusion pressure of 60 mmHg. The patient was nursed 30° head-up and although active cooling was not undertaken, temperature maintained at less 35-37.5°C.

There was initial stability but approximately 24 hours after admission sustained rises in intracranial pressure (ICP) in excess of 25 mmHg were seen, necessitating boluses of sedation, the addition of atracurium by infusion, administration of hypertonic saline, cooling to 35°C and brief periods of hyperventilation to a PaCO2 4.0-4.5 kPa albeit without significant control. Urgent repeat CT brain was undertaken which showed evolution of the contusions with signifiant oedema and loss of both the lateral ventricles and basal cisterns.

On further consultation, neurosurgical colleagues again felt that no immediate surgical option was viable; in particular that attempts to insert and external ventricular drain were unlikely to be successful and that contusionectomy would produce significant disability. The patient was randomised into the RESCUEicp trial and thiopentone infusion started at a rate to produce isoelectrical activity on three lead electroencephalogram.

What are the management options for refractory intracranial hypertension?
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