Fellowship Vivas – Acute Cholangitis, Status Epilepticus and Percutaneous Tracheostomy

Written by Dr Madhuri Anupindi

 

1. 23F admitted following a seizure at work. A collateral history suggests that she has been acting unusually for a few days before she was seen to collapse this morning with a tonic-clonic seizure. Midazolam 5mg IV was administered by paramedics but she continued to seizure. In the ED she was given additional midazolam IV (2mg, 5mg, 5mg) and was loaded with Levetiracetam 1g IV. After 20 minutes she continued to have sporadic seizure activity with a best GCS of 6 and she was intubated (Propofol 180mg and Rocuronium 100mg). She has arrived in your unit on a Propofol infusion at 20mg/hr, ventilated SIMV sats 100% on fio2 0.3. MAP is 75mmHg on no supports, warm and well perfused. Outline your approach to her care over the next 12 hours?

 

My approach would involve an assessment to identify the cause and contributors for her status epilepticus, specific management to treat these causes, management to control the seizures, and supportive management.

Assessment: this would involve history, examination and investigations to identify the cause of her seizures, the differential of which is broad.

History:

• Prior to seizure at work
  • Behaviour changes prior to seizure: aura,
  • Recent travel, infective symptoms, pregnancy, trauma
  • PMx: Known seizure disorder, other co-morbidities including malignancy, endocrine/metabolic disorders (diabetes, renal/hepatic dysfunction, hypothyroidism)
  • Drug use (stimulants, tramadol), or withdrawal (alcohol, benzos, barbituates, baclofen, gabapentin)
  • Medications: OCP, new medications or medication changes, isoniazid, anti-depressants, non adherence to anti-epileptics, medications that lower seizure threshold (beta-lactams, theophylline, lithium, antihistamines)
• Information about seizure
  • What it looked like
  • Any trauma associated

Examination: looking for potential causes and complications from the seizure

• Vital signs, pupils (hippus, dilated, pinpoint, reactivity)
• Focal neurological deficits, clonus, hyperreflexia
• Signs of trauma
• Autoimmune disease/endocrinopathies, pregnancy, vasculitis, track marks
• Neck stiffness/infection
• Signs of ongoing seizure

Investigations

• Bedside: ABG (glucose, electrolytes, lactate), UA, CXR, ECG (prolonged QRS in sodium blockade toxicity), LP
• Bloods: septic screen, organ function and electrolytes, BHCG, autoimmune screen, drug screen, drug levels if on anti-epileptics
• Imaging: CTB, consider MRI
• Special: EEG

 

Management

• Management of status epilepticus: aim to identify ongoing seizure activity and terminate as soon as possible
  • Identification of ongoing seizure activity
    • EEG
    • Consider continuous EEG depending on resources available and if seizure activity not obvious, or ongoing abnormal neurology, or if refractory status epilepticus – titrate to seizure suppression
  • Treatment of status epilepticus: liaise with neurology team
    • Midazolam bolus (0.1mg/kg) then commence infusion and continue propofol infusion  duration of infusions are controversial and depend on whether there is a specific cause identified and if she continues seizing
    • Further levetiracetam 20mg/kg up to a max of 60mg/kg (including what was given in the ambulance) followed by BD dosing
    • If still seizing: valproate 40mg/kg and/or phenytoin 20mg/kg IV and/or lacosamide 10mg/kg (may require multiple-anti-epileptic agents)
    • If remains refractory:
      • Thiopentone coma titrating to burst suppression on EEG
      • Ketamine 1 – 10mg/kg/hr
    • If super-refractory consider:
      • Ketogenic diet
      • Volatile inhalational agents
      • Lignocaine
      • Verapamil
      • Magnesium
      • Hypothermia
    • Identify and treat underlying cause
      • g. antimicrobials if CNS infection, IV magnesium, BP management + delivery if eclampsia, electrolyte replacement if dyselectrolytemia, glucose if hypoglycaemia, sodium bicarbonate if sodium channel blocker
    • Neuroprotective measures, aim to avoid reducing seizure threshold
      • Optimise BSL/electrolytes, normotension, normoxia, normocapnoea

Supportive

• Family update
• PPI
• Nutrition: NG feeds, aperients
• Lines and access: arterial and central line, IDC
• Chemical DVT prophylaxis if nil contraindications

 

List the prognostic factors for outcome from SE

• Older age
• Multiple co-morbidities
• Aetiology of SE:
  • better outcome with SE secondary to previously diagnosed epilepsy, alcohol withdrawal
  • worse outcome if secondary to stroke, hypoxic brain injury, unknown cause or infection
• Focal neurological signs at onset
• Increased duration of SE
• Complications from SE or from ICU treatment

 

Outline the role of continuous EEG in the management of status epilepticus in the ICU

 

The exact role of cEEG within the ICU is still being elucidated and depends on the patient population and the resources available at your hospital.

Rationale:

• Prognosis worsens with increased time spent in SE  timely identification and management of same is thus crucial
• Intermittent EEG only captures a short period of time, during which the patient may not be having seizure activity
• Continuous EEG increases the likelihood of detecting non-convulsive seizure activity and can also be used to titrate sedative agents and anti-epileptic therapy in real time, thus hopefully minimising adverse effects from unnecessary or prolonged treatment

Patient population: no clear guidelines but recommendations (American Clinical Neurophysiology Society and ESCICM) include:

• Persistently impaired consciousness that persists after initial treatment of seizures as non convulsive seizures are relatively common in this population
• Clinical paroxysmal events suspected to be seizures to clarify if ictal or non-ictal (balancing risks of treatment with risks of ongoing seizure activity) e.g. paroxysmal autonomic episods, nystagmus
• Refractory status epilepticus or suspected non-convulsive epilepticus – both to identify same and to evaluate response to therapy
• If using neuromuscular blocking agents or deep sedation

Resources:

• Will depend on access to continuous EEG in your unit  not only the equipment but having trained personnel who are able to interpret and act on the data
• Is resource intensive and not readily available in most units and there are many sources of potential artefact within the ICU

 

What are the complications associated with the management of SE in the ICU

Complications secondary to medications used to treat SE:

• Cardiac:
  • Hypotension– e.g. secondary to sedation , phenytoin infusion, barbituates
  • Arrhythmias – potassium shifts secondary to thiopentone, phenytoin, ketamine vasopressors used to counteract sedation PR interval prolongation with higher doses lacosamide
  • Propofol infusion syndrome
• Neuropsychiatric adverse effects: agitation, somnolence, behavioural changes, neuropathy, ataxia secondary to AEDs
• Immune: Hypersensitivity reactions, DRESS secondary to anti-epileptics, immunosuppression secondary to thiopentone
• Metabolic: Hepatic toxicity, hyperammonemic encephalopathy
• Haem: platelet dysfunction secondary to valproate

Complications secondary to SE:

• CNS: Intra-cranial hypertension, neuronal injury
• Resp: Neurogenic pulmonary oedema, aspiration pneumonitis
• Cardiac: Takatsubo’s cardiomyopathy, autonomic dysfunction and arrhythmias
• Metabolic: Rhabdomyolysis and renal failure if prolonged seizures, Pyrexia
• Haem: DIC
• Trauma secondary to seizures e.g. tongue biting, fractures, shoulder dislocation

General complications secondary to ICU stay:

• CNS: delirium, PTSD, critical illness associated weakness
• Resp: vocal cord dysfunction if prolonged intubation, atelectasis
• Haem: Venous thromboembolism
• Infections: ventilator acquired pneumonia, line associated, sinusitis etc as well as increased susceptibility if immunosuppressed (either with high dose thiopentone or with immunosuppression if autoimmune encephalitis)
• Other: Pressure areas, risks of polypharmacy, complications from line insertion

 

Briefly outline the rationale and evidence for hypothermia in the management of refractory SE

Therapeutic hypothermia for refractory SE remains controversial and is generally only considered in super refractory cases. Refractory SE has a high associated morbidity and mortality, and remains challenging to treat.

Rationale:

• Hypothermia has anti-epileptic properties, decreases cerebral metabolic demand and oxygen consumption, reduces excitotoxicity and increases the seizure threshold
• Potentially decreases secondary injury: decreases production of oxygen free radicals and neuronal apoptosis, decreases CP, preserves blood brain barrier

Evidence:

• Initially largely from animal models
• Main trial is HYBERNATUS: 2016 NEJM in 268 patients from 11 French ICUs with convulsive SE requiring mechanical ventilation
  • Randomised to 32-34 degrees versus normothermia
  • Primary outcome was GOS of 5 (survival with no or minimal neurological deficits)
  • There was no significant difference in primary outcome or secondary outcomes (mortality, seizure duration, length of stay etc).
  • Number of reported adverse events higher in the hypothermia group but progression to EEG confirmed status was lower
  • Several limitations: used in all patients with status requiring invasive ventilation rather than in refractory cases which is not standard (only 25% were actually in status at time of randomisation), ?utility of having just 24 hours of hypothermia regardless of whether patient was still in status, target temperature in hypothermia group was attained at a median of 5.2 hours

 

2. You are asked to review a confused 65-year-old female with ischaemic heart disease, chronic obstructive airways disease and atrial fibrillation in the Emergency Department, who has presented with abdominal pain and vomiting. Her vital signs, after 4 litres 0.9% saline intravenously are as follows: Temperature 39.5oC, respiratory rate 30 breaths/min SpO2 92% on 15 L/min oxygen via a reservoir mask, heart rate 120 beats/min (atrial fibrillation), blood pressure 88/48 mmHg. She is icteric, has right upper quadrant tenderness and is mildly confused. What is your differential diagnosis?

 

I think this lady has biliary sepsis – most likely ascending cholangitis.

Other differentials include

Infective:

• Cholecystitis
• Hepatitis
• EBV or CMV
• Liver abscess
• Sepsis with multi-organ failure

Non-infective

• Inflammatory: acute pancreatitis with biliary obstruction, decompensated liver failure e.g. secondary to underlying alcoholic liver disease or hepatitis, perforated viscus with associated intra-abdominal sepsis
• Drug overdose: paracetamol, MDMA, amanita phalloides, idiosyncratic reactions to drugs
• Vascular: Budd Chiari, hepatic arterial ischaemia, intra-hepatic haemorrhage (may be on anticoagulation due to AF)
• Auto-immune: HLH
• Cardiogenic: right heart failure – may be ischaemic, PE, myocarditis, secondary to pulmonary hypertension from severe COPD, cardiogenic shock with biventricular failure

 

Briefly outline how you would further evaluate this lady’s presentation.

This would involve a targeted history and investigations aimed at ascertaining the cause of this lady’s illness, considering the differentials discussed earlier. Priority would be for imaging o the biliary system given her presentation.

 

History

• Further info about presenting complaint: associated infective symptoms, timing of deterioration, characteristics surrounding abdominal pain, bowel/bladder symptoms and change in colour, unwell contacts, recent travel
• BG: history of gallstones or pancreatitis, ETOH/drug history, allergies, IVDU, tattoos, malignancy, severity of COPD and ischaemic heart disease, previous history of biliary disease/procedures
• Medications: anticoagulants, medications known to have caused idiosyncratic acute liver failure (amoxicillin, doxycycline, NSAIDs, TCAs, statins, phenytoin)

Investigations:

• Bedside: ECG (ischaemia, right heart strain), ABG (lactate – shock, liver impairment, oxygen/ventilatory status, electrolytes, acidosis, BSL), Urine MCS (infection, bilirubin)
• Bloods: FBC (haemoglobin – bleeding, WCC – leucocytosis, platelets – liver disease, HLH), UEC (renal function), LFTs (liver function), coags (anticoagulants, liver failure), troponin (ischaemia), ferritin (if suspicions re HLH), ETOH/paracetamol level (if suspicion of overdose/toxin), blood cultures (septic screen), lipase (pancreatitis)
• Imaging: CXR (free air, cause of hypoxia), US of gallbladder if readily available otherwise CT abdomen, TTE (cardiac function)

 

An US of her abdomen shows a dilated common bile duct and an enlarged, oedematous, gallbladder. Outline your key management principles for this patient.  

This lady most likely has acute cholangitis with signs of multi-organ impairment and requires urgent stabilisation and management targeted at source control with biliary decompression.

My management principles include:

• Optimisation of haemodynamics
  • Requires central access, arterial line, IDC, NGT, full monitoring in situ
  • Not for further IV fluids currently (has had 4L and is hypoxic)  start noradrenaline aiming MAP > 65, add vasopressin if high dose noradrenaline required
  • Nil specific treatment for AF currently except ensure electrolytes optimised, not for anticoagulation, consider amiodarone or digoxin if AF with RVR despite source control and resolution of fever
• Optimisation of respiratory parameters
  • Hypoxic with respiratory distress requiring a NRBM  will likely require intubation given shock, respiratory status, confusion and likelihood of needing a procedure (ERCP or percutaneous), aim sats => 92%, normocapnoea (or baseline co2 if co2 retainer), continue regular inhalers for COPD
  • Can place on HFNP to pre-oxygenate or temporise or continue NRBM depending on patient status, unlikely to be suitable for NIV given vomiting and confused
• Source control
  • Start broad spectrum antibiotics: Tazocin  rationalise depending on culture results
  • Urgent discussion with gastro and expedite ERCP +/- sphincterotomy or percutaneous decompression
• Logistics and supportive care
  • Requires admission to ICU  potentially via OT for decompression depending on timing that can be facilitated
  • Remain NBM currently and review regularly regarding timing of nutrition, aim BSL 6 – 10
  • Temperature management: stat dose paracetamol +/- regular depending on LFTs, ice packs if intubated aiming normothermia
  • Monitor organ function, mechanical DVT prophylaxis for now, PPI

 

3. Obese 65M ventilated person has been ventilated for 10 days with CAP. Describe the preparation, indications, contraindications and equipment required prior to commencing a percutaneous tracheostomy.

 

Indications: ANZICS consensus statement

• Airway maintenance
  • Upper airway obstruction
  • Inability to protect the airway
• Prolonged ventilation
  • Prolonged dependence on mechanical ventilation (actual or anticipated)
  • Aid in secretion management
  • Permanent or long term airway access in traumatic or neurological diseases

 

Contraindications:

• Anatomical issues
  • Anatomical anomalies: anterior neck mass, large goitre, aberrant vessel anatomy
  • Difficult landmarks: significant obesity, short neck, previous neck surgery or radiotherapy distorting anatomy
  • Airway: difficult airway or inability to safely manage airway
  • Neck: unstable c spine injury, inability to extend head
• Pathology
  • Severe hypoxic respiratory failure
  • Infection at site of insertion
  • Severe haemodynamic instability
  • Coagulopathy
  • Unsurviveable illness
• Lack of consent

 

Preparation

• Patient
  • Consent obtained
  • Review indications, anatomy of patient, airway grade, resp/haem/coag status, and ensure no contraindications to tracheostomy
  • Fasted: nil feeds/solids last 6 hours, no anticoagulants, DVT prophylaxis WH that morning
  • Pre-oxygenated: fio2 1 on ventilator, appropriate ventilator settings for paralysed patient
  • Full monitoring including sats, BP, ECG, etco2
  • Sedated and paralysed
  • Positioned appropriately: supine, neck extended
• Location
  • In ICU, adequate space and lighting
• Staff
  • In our institution requires presence of two intensivists
  • Airway: person managing airway, monitoring and anaesthetic, must be skilled at managing airway, intubation and responding to deteriorations/emergencies
  • Bronchoscopy: doctor managing bronchoscopy to identify correct position of needle insertion, guide wire placement and trache position
  • Proceduralist: senior trainee and/or intensivist with appropriate experience
  • Nursing staff x 2: monitoring, runner, helping with equipment
• Equipment: all available at bedside
  • Airway equipment
    • Airway trolley: equipment for re-intubation if required, adjuncts and for emergency airway access
    • Bronchoscopy and laryngoscope
    • Emergency trolley
  • Tracheostomy equipment
    • Insertion kit, sterile field, lignocaine with adrenaline, trache dressings
  • Drugs
    • Sedation and paralysis
    • Emergency drugs: vasopressors, intubation meds, medications in event of arrest

 

List the advantages and disadvantages of a percutaneous tracheostomy compared to a surgical tracheostomy:

 

Advantages

• Logistics: done at bedside so no transport required, does not require surgeon, anaesthetist or OT time, less expensive, faster to perform
• Decreased incidence of bleeding, stoma breakdown, tracheal stenosis and of infection
• Smaller incision  better cosmesis

Disadvantages

• Higher incidence of anterior tracheal wall injury and posterior wall perforation
• If significant procedural complication requires surgical attendance and transfer to OT
• No diathermy available in case of bleeding
• No stay sutures
• No true direct visualisation except for needle/guidewire if using bronchoscopic gudiance
• Unique risks due to insertion technique: wire loss/kinking or fracture, damage to bronchoscope, tracheal ring fracture, cricoid fracture, false passage, conversion to open, oesophageal injury, lateral placement of tracheostomy