OXY’s LOG – ‘That tricky fella, human error…’

‘Errare humanum est’ 

Adapted by Alexander Pope1 in 1711 into the famous quote: ‘To err is human, to forgive divine.’

Case: A MVA victim (later retrieved by GSA-HEMS) comes into a rural trauma unit with a head injury and facial fractures. They need intubating. There are three other victims from the same MVA on their way in.  One of our specialists happens to be working an ED shift with an experienced GP anaesthetist doing a locum shift. The intubation is delegated to the GP anaesthetist so that the ED consultant is free to manage the other three victims on their arrival. The GP mistakenly intubates the oesophagus. There is no CO2 trace and no chest movement. On questioning the GP anaesthetist suggests there is a problem with the capnography module on the monitor and asks for a colour-metric CO2 detector. After this device has also revealed no EtCO2, the ED consultant removes the tube and correctly intubates the trachea. The patient was pre-oxygenated appropriately and did not desaturate during the entire intubation episode. 

Challenge: To acknowledge that we will all suffer from human error, and think about ways to reduce this leading to patient harm.

Learning points: High technology systems have many defensive layers to avoid adverse events: some are engineered (alarms, automatic shutdowns, some rely on people (medics, pilots) and others depend on procedures and administrative controls2.

In medicine their function is to protect patients becoming victims. Nearly all adverse events involve a combination of active failures and latent conditions.

Active failures are like mosquitoes: they can be swatted one by one, but they will keep coming. The best remedies are to create more effective defences e.g. to drain the swamps in which they breed. The swamps, in this case, are the latent conditions. Understanding this concept leads to proactive rather than reactive risk management.

Human error can be viewed in two ways: the person approach and the system approach. The basic premise to the ‘system approach’ model of human error is that humans are fallible and  errors are to be expected, even in the best organisations. Counter measures are based on the assumption that though we cannot change the human condition, we can change the conditions under which humans work. The important issue is not who blundered, but how and why the defences failed2

The ‘person approach’ to error focuses on the unsafe acts – the errors – of people at the sharp end. People exhibit three error types:

Mistakes (planning stage) occur when the steps in the plan are adhered to but the plan was wrong. Our case – that the GP anaesthetist performed the intubation without possessing the proper skills. 

Lapses (storage stage) are associated with our memories; when someone has failed to do something because of a lapse in memory or attention e.g. skipping a step on a check list. Our case – the GP anaesthetist forgetting to place the suction catheter under the pillow and so cannot remove the blood in the airway which is blocking their view. 

Slips (execution stage) are generally observable actions that are not in accordance with a plan e.g. mis-keyed command. Slips are most often associated with the execution phase of cognition3. Our case – the GP anaesthetist not trusting the CO2 monitors to be correct. 

There were lots of safety measures in place to prevent this patient coming to harm e.g. well equipped ED bed-spaces, trained staff, protocols, pre-oxygenation, alternative ways to check ventilation, different ways to monitor EtCO2, senior supervision and questioning and re-checking steps.  

Human reliability specialists now widely uphold the idea that productive strategy for managing human error should focus upon controlling the consequences rather than striving for the elimination of this error3. And effective error management depends crucially on establishing a reporting culture4.

Without a detailed analysis of mishaps, incidents and near misses, we have no way of uncovering recurrent error traps. The complete absence of such a reporting culture within the Soviet Union contributed crucially to the Chernobyl disaster5

Final thought: Limiting the incidence of dangerous errors will never be wholly effective but resilient organisations create systems that are able to tolerate the occurrence of errors and contain any possible damage. Comprehensive management programmes target: the person, the team, the task, the workplace and the institution as a whole6. They expect individuals to make errors and train their workforce to recognise and recover them. Their staff continually rehearse scenarios where there is potential for failure (any of this sound familiar?)

References: 

1. Pope, A., J. W. Croker, et al. 1871. The Works of Alexander Pope, J. Murray.

2. Reason, J. 2000. “Human error: models and management.” Bmj 320(7237): 768-770.

3. Hollnagel, E. 1993. “The phenotype of erroneous actions.” International Journal of Man-Machine Studies 39(1): 1-32.

4. Reason, J. 1997. Managing the risks of organizational accidents. Aldershot: Ashgate.

5. Medvedev G. 1991. The truth about Cher nobyl. New York: Basic Books.

6. Reason J. Human error. New York: Cambridge University Press, 1990.

“Cuiusvis hominis est errare, nullius nisi insipientis in errore perseverare”

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Clinical Governance Day 9th May 2012

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OXY’s LOG – ‘Sadly just too big a hole in that pearl…’

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 elsewhere.

4.1.1 All cardiac arrest patients should be intubated without anaesthetic drugs.

4.2.1 Unless the possibility of tension pneumothorax can be reliably excluded, bilateral open thoracostomies should be made2. Needle thoracocentesis may be performed initially for reasons of access or expediency but these should not be considered to provide definitive pleural drainage.

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:

1. Wise D, Davies G, Coats T, Lockey D, Hyde J, Good A. Emergency thoracotomy: “how to do it” Emergency Medicine Journal 2005;22:22-24.

2. Massarutti D, Trillò G, Berlot G, Tomasini A, Bacer B, D’Orlando L, Viviani M, Rinaldi A, Babuin A, Burato L, Carchietti E. Simple thoracostomy in prehospital trauma management is safe and effective: a 2-year experience by helicopter emergency medical crews. Eur J Emerg Med. 2006 Oct;13(5):276- 80.

3. Davies GE, Lockey DJ. Thirteen Survivors of Prehospital Thoracotomy for Penetrating Trauma: A Prehospital Physician-Performed Resuscitation Procedure That Can Yield Good Results. J. Trauma. 2011 May;70(5):E75-8.

4. Rhee PM, Acosta J, Bridgeman A, Wang D, Jordan M, Rich N. Survival after emergency department thoracotomy: review of published data from the past 25 years. J Am Coll Surg. 2000 Mar;190(3):288-98.

“Amat Victoria Curam”

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OXY’s LOG – ‘Sux it, don’t stroke it…’

Succinylcholine and the hemiplegic patient

(This is a follow-up post to a previous blog regarding Suxamethonium and neurological disorders).

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:

1. Smith, R. B. and Grenvik, A. 1970. “Cardiac arrest following succinylcholine in patients with central nervous system injuries.” Anesthesiology 33(5): 558.

2. Gronert, G.A., Theye, R.A. 1975. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology; 43:89–99.

3. Martyn, J.A.J., White, D.A., Gronert, G.A., Jaffe, R.S., Ward, J.M. 1992. Up-and-down regulation of skeletal muscle acetylcholine receptors: Effects on neuromuscular blockers. Anesthesiology; 76:822–43.

4. Brown, J., Charlton, J. et al. 1975. “A regional technique for the study of sensitivity to curare in human muscle.” Journal of Neurology, Neurosurgery & Psychiatry 38(1): 18-26.

5. Martyn, J. A. J. and M. Richtsfeld 2006. “Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms.” Anesthesiology 104(1): 158.

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.

7. Thomas, E. T. 1969. “Circulatory collapse following succinylcholine.” Anesthesia & Analgesia 48(3): 333-337.

8. Al-Khafaji, A.H., Dewhirst, W.E., Cornell, C.J., Quill, T.J. 2001. Succinylcholine- induced hyperkalemia in a patient with mucositis secondary to chemotherapy. Crit Care Med 2001; 29:1274–76.

9. Matthews, J.M. 2000. Succinylcholine-induced hyperkalemia and rhabdomyolysis in a patient with necrotizing pancreatitis. Anesth Analg 2000; 91:1552–4.

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’

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OXY’s LOG – ‘It totally sux…’

Suxamethonium and neurological disorders

Case: A relatively innocuous case concerning the transportation of a Parkinson’s diseasesufferer lead onto that age-old discussion about our old friend the depolarising neuromuscular blockerand 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 indicated4. 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”

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OXY’s LOG – ‘Please put me to sleep…’

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.

Crit Care Med. 2011 Dec;39(12):2743-51

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OXY’s LOG – ‘Not your typical anti-psychotic’

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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Clinical Governance Day 28th March 2012

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Clinical Governance Day 14th March 2012

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Special Casualty Access Team training

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