Clam shell thoracotomy – Indications and outcomes
Case: A multiple gun shot wound victim was found at the roadside barely conscious. He was intubated, ventilated and given bilateral thoracostomies by our HEMS crew. He went into cardiac arrest and so the team decided to perform an open thoracotomy1. His pericardium was full of clot and when opened revealed a linear tear in his right ventricle. During bimanual cardiac compressions his heart felt empty. The extent of his injuries, including the one described above, were judged to be an ELE (Extinction Level Event).
Challenge: What are the indications and reported outcomes for prehospital thoracotomy?
Learning Points: Here’s an excerpt from the Traumatic Cardiac Arrest HOP:
4.6.3. Penetrating Trauma
4.6.3.1 Thoracic or upper abdominal penetrating injury resulting in cardiac arrest should initially be managed as in 4.1.1 and 4.2.1 (see below). If there are signs of life withint a 10 min window prior to team arrival and there is no response to intubation / bilateral thoracostomy, a clamshell thoracotomy should be made with the specific purpose of relieving cardiac tamponade, controlling a cardiac wound(s) and providing internal cardiac massage. A detailed description of this technique is beyond the scope of this HOP but is clearly explained elsewhere1 .
Anterior bilateral thoracotomy (Clam Shell): Provides excellent exposure of the heart and mediastinum. The idea is that a non-cardiothoracic surgeon should be able to access the pericardium with 2-3 mins.
Indication: Penetrating chest or epigastric trauma associated with cardiac arrest.
Contraindications: Cardiac arrest for greater than 10mins (or if there is still a cardiac output?!). Evidence from one case series suggested a poor neurological outcome for those patients who were in cardiac arrest for anymore than 10 mins3.
It is important to have realistic expectations. This procedure best tackles a single pathology – cardiac tamponade with a controllable wound in the heart. If the underlying injury is any more complex, a good outcome is unlikely. A 25 year review of ED thoracotomies conducted in 2000 highlighted survival rates based on mechanism of injury. In descending order: 19.4% for isolated cardiac wounds, 16.8% for stab wounds, 4.3% for gunshot wounds and 1% for blunt trauma4.
Summary: Clam shell thoracotomy is a useful tool in the desperate attempt to resuscitate penetrating trauma victims who are in extremis. If applied selectively, this procedure can be lifesaving.
References:
“Amat Victoria Curam”
Succinylcholine and the hemiplegic patient
The hemiplegic patient does indeed present a risk. There are a number of case reports of stroke patients arresting on the end of a syringe of sux1,2,3.
Brown and Charlton4 studied 12 hemiplegic patients and observed larger muscle action potentials and smaller fade ratios when compared with the normal side. Interestingly dennervation causes a more pronounced response than immobilisation5. Age or severity of the stroke did not seem to correlate with muscle activity.
There is now evidence that a pathological isoform of the acetylcholine receptor (AChR), neuronal (nicotinic) 7AChR, not usually found in normal adult muscle, is expressed and up-regulated in muscle during denervation6. This up-regulation of AChRs, when depolarized with succinylcholine, leads to an efflux of intracellular potassium into the plasma causing acute hyperkalaemia.
The period on vulnerability to hyperkalaemia for hemiplegic patients is not well defined but case reports have suggested the period to be as early as one week5 and as late as six months1.
Others:
Some of the other conditions reported to cause hyperkalaemia with succinylcholine have included: gastrointestinal mucositis8, necrotizing pancreatitis9, catatonic schizophenia10, meningitis11, and purpura fulminans12.
Thoughts:
I guess this adds more weight to the argument to use Roc in many more time-critical intubation situations.
References:
6. Fischer, U., Reinhardt, S., Albuquerque, E.X., Maelicke, A. 1999. Expression of functional alpha7 nicotinic acetylcholine receptor during mammalian muscle development and denervation. Eur J Neurosci; 11:2856–64.
10. Cooper, R.C., Baumann, P.L., McDonald, W.M. 1999. An unexpected hyperkalemic response to succinylcholine during electroconvulsive therapy for catatonic schizophrenia. Anesthesiology; 91:574–5.
11. Hansen, D. 1998. Suxamethonium-induced cardiac arrest and death following 5 days of immobilization. Eur J Anaesthesiol; 15:240–1.
12. Kovarik, W.D., Morray, J.P. 1995. Hyperkalemic cardiac arrest after succinylcholine administration in a child with purpura fulminans. Anesthesiology; 83:211–3.
‘Qui rogat, non errat’
Suxamethonium and neurological disorders
Case: A relatively innocuous case concerning the transportation of a Parkinson’s disease1 sufferer lead onto that age-old discussion about our old friend the depolarising neuromuscular blocker2 and which weird and wonderful neurological or neuomuscular problems it could or should not be used for.
Challenge: To use sux or not to use sux, that is the question.
Learning points: The figure below highlights those conditions where careful consideration of the use of Sux is indicated3 4. Your next line of defence is Rocuronium. Given in sufficient doses, Roc has as quick an onset time as Sux in a practical setting5.
Wanky disclaimer: Suxamethonuim causes some increase in K+ in ALL that are given it. Therefore any condition that might result in an increased K+ can have a further surge in K+once given the drug3.
Reference:
1. Parkinson’s Disease and Anaesthesia
Indian J Anaesth. 2011 May-Jun; 55(3): 228–234 Free full text
2. Suxamethonium article from frca.co.uk
3. Suxamethonium article from Update in Anaesthesia
4. Information for Health Professionals: Suxamethonium Chloride Injection B.P.
5. Rocuronium versus succinylcholine for rapid sequence induction of anesthesia and endotracheal intubation: a prospective, randomized trial in emergent cases.
Anesth Analg 2005; 101:1356–61 Free full text
“Quod medicina aliis, aliis est acre venenum”
Analgesia for the head injured patient
Case: A young adult attempted hanging victim with a decreased GCS was intubated and ventilated at a referring hospital. He required interhospital retrieval to a tertiary care facility. On arrival the team noted the patient was hypertensive, tachycardic and there apppeared to be patient-ventilator dysynchrony. He was sedated with midazolam only.
Challenge: How to achieve cerebral perfusion and neuro-protection.
Learning points: Clearly this patient needs to be properly sedated, but we must be mindful of the need to perfuse this potentially injured brain. It is common to aim for a cerebral perfusion pressure (CPP) of 60mmHg. If we initially assume a ICP of 20mmHg, then this patient needs a MAP 80mmHg. This patient’s cardiovascular observations will certainly tolerate an increase in sedation and his ICP and metabolic rate are not being helped by inadequate sedation. High arterial CO2 and raised intra-thoracic pressures generated by ‘fighting’ the ventilator should also to be avoided in this head injured patient.
“5.2 The ideal sedation regimen provides adequate analgesia and should be easily titratable to effect with minimal haemodynamic response”.
Adding fentanyl and increasing the midazolam infusion brought the cardiovascular parameters down to more reasonable levels and the patient’s ventilation settled, all benefiting the injured brain.
Here’s the full excerpt from the Neuroprotection Helicopter Operating Procedure:
5. Sedation and Paralysis
5.1. In order to avoid spikes in ICP it is imperative that the patient be adequately analgesed and sedated.
5.2 Movement between stretchers and changing ventilation circuitry are events which may cause patients to cough, gag or suffer arousal unless very well sedated. The ideal sedation regimen provides adequate analgesia and be easily titratable to effect with minimal haemodynamic responses.
5.2.1. Fentanyl is an effective analgesic with sedative properties and is cardiovascularly stable.
5.2.2. Midazolam has anticonvulsant properties which may be desirable.
5.2.3. Propofol is rapidly titratable, reduces cerebral metabolism and allows for neurologic assessment shortly after weaning. It may cause more cardiovascular depression.
5.2.4. Ketamine provides excellent analgesia as well as dissociative sedation. Historical concerns about its use in patients with raised ICP are unfounded, as it generally supports MAP and hence CPP.
5.3. The use of paralytic agents should be considered in all patients with raised ICP following adequate analgesia and sedation. Whilst muscle relaxants can mask clinical signs of seizure activity they are effective in preventing coughing and gagging and patient-ventilator asynchrony which can aggravate raised ICP.
4.4 Blood Pressure Manipulation
4.4.1 General Recommendations
Cerebral autoregulation in the injured brain may be impaired and a target CPP of 50- 70mmHg is recommended. However, unless an external ventricular drain (EVD) with pressure monitoring is present it is not possible to determine CPP. Blood pressure targets must therefore be empirically chosen and should be discussed with the receiving neurosurgical team.
Reference: Sedation for critically ill adults with severe traumatic brain injury: A systematic review of randomized controlled trials.
Quetiapine Overdose
Case: A young adult male was found comatosed after suspected overdose. His regular medications included quetiapine. He required interhospital retrieval to a tertiary care facility. He was intubated and ventilated but required only minimal sedation.
Challenge: To discover the issues surrounding quetiapine overdose.
Learning points: Quetiapine is an atypical antipsychotic used in the treatment of schizophrenia. The main clinical findings in quetiapine overdose (resulting from α-adrenergic and histamine receptor blockade) are hypotension, tachycardia, and coma. The potentially life-threatening consequences from overdose include QT prolongation and respiratory depression.
The only deaths that have been reported have occurred in patients with other co-morbidites.
There is no specific antidote, and quetiapine overdose is managed by appropriate supportive measures. Ventilation is often required. Out of all the anti-psychotics, quetiapine causes the most hypotension in overdose and the patient should be monitored closely for cardiac dysrhythmias.
Reference: Ngo A, Ciranni M, Olson KR. Acute quetiapine overdose in adults: A 5-year retrospective case series. Annals of Emergency Medicine 2008; Volume 52, Issue 5, Pages 541-547.
10.1016/j.annemergmed. 2008.03.016
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