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Case Study 64 Cva Firearms

by Alan Batt. Last modified: 03/03/14

Patient & Apparent Chief Complaint

A 68 year old male presents to ambulance crew through emergency call after falling from his bicycle at an unknown speed.

History

Patient was cycling on quiet country road when he fell from his bicycle. He was not wearing a helmet at the time. His friend found him semi-conscious on the road. He was placed sitting in a car that stopped to help where he was still sitting on arrival of ambulance crew.

Initial Clinical Findings

  • Airway – partially obstructed, large amounts of vomit evident
  • C Spine – suspected (MOI: fall, altered LOC)
  • Breathing – regular
  • Circulation – Pulse present, regular, skin colour pale, cap refill delayed (>2 sec)
  • Disability – LOC before ambulance arrival; patient experiencing periods of lucidity, alternating with responding to voice

Clinical Impression

Head injury secondary to fall

AMPLE History

  • A No known allergies
  • M Currently taking ant-hypertensive medications
  • P History of hypertension, investigated for right sided weakness 2/52 previous to event
  • L Last oral intake lunch earlier that day
  • E Found semi-conscious on road after fall from bike, no evidence of collision with vehicle

Observations – Prehospital

  • Pulse rate 58bpm
  • Pulse rhythm Regular
  • ECG rate 58
  • ECG rhythm Sinus bradycardia
  • Resp rate 20 per minute, normal, regular
  • Resp quality Equal air entry bilaterally
  • SaO2% 99% on 15lpm via NRB
  • Cap Refill >2secs
  • BP 136/101
  • Pupils Left size 3, reactive. Right unreactive, (damaged in surgery)
  • GCS 15/15 (E4, V5, M6)
  • BGL 7.1mmol/l

Prehospital care & management

O2 @15lpm commenced via non-rebreather mask. Cervical collar applied. Patient extricated from vehicle via rapid extrication, as vomiting profusely, unable to manage airway adequately. Secured to longboard, transferred to ambulance. Suction provided as patient’s level of consciousness began to deteriorate, snoring respirations evident.

En-route, GCS reduced to 3/15, patient unresponsive. OPA inserted, not tolerated. Vomiting profusely, incontinent of urine, decorticate posturing evident. Transported in right lateral position to allow for airway management. On arrival at ED  patient exhibiting decerebrate posturing.

In-hospital care & management

Patient triaged as Category 1 (Life-Threatening Condition) with Head Injury, Spinal Injury, Unconscious. Brought directly to Resus room. Aggressive airway management commenced. Patient sedated, paralysed and intubated (RSI). Urinary catheter inserted. Blood tests taken.

Clinical Findings

No overt head injury evident. Query cause of fall. Sent for CT Brain. Large hypertensive bleed found on scan. Patient sent to ICU on ventilator. Patient diagnosed with severe hypoxic brain injury secondary to hypertensive CVA. Family and healthcare provider joint decision to turn off ventilatory support 26 hours post-event.

Identification of all interventions initiated and rationale

  • Oropharyngeal airway – to protect the airway due to decreased level of consciousness
  • Suction – to clear the airway of vomit due to patient’s inability to maintain own airway
  • Pulse oximetry – to monitor oxygen saturation levels in the blood
  • Supplemental oxygen – to re-oxygenate patient
  • Cervical collar and longboard – to provide support and protection to cervical spine due to serious mechanism of injury suggestive of spinal injury
  • 3 Lead ECG – to identify any life-threatening arrhythmias
  • 12 Lead ECG – to identify any life-threatening arrhythmias or ECG changes indicative of myocardial damage (primary cause of fall, secondary to hypoxia etc.)
  • CXR – to identify pneumothorax, pleural effusion etc. that may increase morbidity
  • Blood tests – to identify any electrolyte imbalances etc.
  • Urinary catheter – to monitor urinary output to ensure adequate renal function
  • CT Brain – to identify any cerebral haemorrhage or infarct that may be indicative of primary cause of fall.

Learning Outcomes

Rapid Sequence Intubation (RSI)

Rapid Sequence Induction is the use of a sedative with a paralytic agent to facilitate endotracheal intubation in an aggressive/combative/non-compliant patient who requires airway management (such as in severe head injuries). This is an intervention currently outside the scope of practice for many Paramedics worldwide, unless operating at a Critical Care or Intensive Care Paramedic level.

There are many studies and articles detailing both the benefits and disadvantages to performing RSI pre-hospital in the hands of Paramedics – non-anaesthetic practitioners have a higher tracheal intubation failure rate during pre-hospital RSI. (Ochs et al., 2003; Wang et al.; 2001; Sloane et al., 2000; Dunford et al., 2003; Fullerton et al., 2011; Bernard et al., 2014).

Wang et al. (2001) comes to the conclusion that prehospital RSI can be harmful to patients with TBI. Sloane et al. (2000) found no difference in outcomes between prehospital and intrahospital RSI outcomes, with similar success and complication rates. RSI is an approved skill for Paramedics in certain jurisdictions such as San Diego, and 29 of the states in the US have medication assisted intubation protocols for use by Paramedics (Gausche-Hill, 2004)

Severe traumatic brain injuries are associated with aspiration, bradycardia, hypoxia and further complications. Wang et al. (2001) also pose the question “Should we be intubating prehospital at all?”. This is an area of constant debate in the past few years, and opinions are mixed.

Restrictions on RSI protocols could include, but are not limited to:

  1. That it be restricted to experienced Paramedics with a minimum qualification period
  2. That it be restricted to Paramedics that complete a required training programme, including a certain number of successful intubations in an operating theatre in addition to their initial training
  3. That these individuals maintain a certain number of intubations and medication-assisted intubations annually
  4. That there be strict protocols on its’ implementation as per clinical guidelines
  5. That is always a secondary fallback device available when undertaking RSI, such as a supraglottic airway device (LMA, Combitube etc.) in case of failed intubation

The issues that arise with authorising RSI for prehospital use by Paramedics include prolonged scene times, induced bradycardia, raised ICP and oxygen desaturation to name a few. Additional medications would also need to be added to the list of approved medications for many practitioners in order to allow for RSI to be introduced. The implementation of this intervention in any jurisdiction needs to be investigated regarding feasibility, training requirements, syllabus construction, cost implications etc.

Abnormal Posturing

Abnormal posturing (pathological posturing) can often be seen in patients with a serious CNS insult/injury such as that associated with a head injury, CVA, CNS infection or other cause. Normally, when a muscle contracts, the muscles on the opposite side of the joint provide some resistance to contraction. Abnormal posturing occurs when damage to the CNS (brain or spinal cord) results in complete or partial lack of opposition to muscle contraction in various muscle groups.

There are 2 types of posturing: decorticate and decerebrate.

Decorticate Posturing

This involves rigidity, flexion of the arms, clenched fists, and extended legs. The arms are bent inward toward the body with the wrists and fingers bent and held on the chest. This type of posturing implies severe damage to the brain.

Decerebrate Posturing

This involves rigid extension of the arms and legs, downward pointing of the toes, and backward arching of the head. A severe injury to the brain at the level of the brainstem is the usual cause of decerebrate posture.

Opisthotonos

This is a condition of abnormal posturing that involves rigidity and severe arching of the back, with the head thrown backward. If a person with opisthotonos were laid on his or her back, only the back of the head and the heels would touch the supporting surface. This often accompanies decerebrate posturing in severe CNS insult. (Elling et al., 2007)

A patient may alternate between different postures as their condition worsens/improves. According to Russell and Triola (1995) and Weiner and Goetz (2004) in general, patients with decorticate posturing have a better prognosis than patients who exhibit decerebrate posturing, although decerebrate posturing can be seen with some forms of reversible yet severe encephalopathies.

Methods to reduce increased ICP associated with endotracheal intubation

Endotracheal intubation is the definitive method of securing an airway in a patient with a severe head injury. However, endotracheal intubation is linked with a marked raise in ICP for a duration of 3-5 minutes. The exact effect this transient raise in ICP has on primary and secondary brain injury is unknown, however it is widely believed that it has a detrimental effect on secondary brain injury, due to cerebral hypoperfusion.

The use of IV lidocaine prophylactically prior to intubation (as in RSI) is recommended by Salhi & Stettner (2007) and various other authors. However, there are other authors and studies such as Robinson & Clancy (2001) who indicate that the use of IV lidocaine to mitigate rises in ICP related to intubation should not become accepted practice until further studies are carried out.

Hyperventilation is another technique that can be used to decrease ICP. However, this should be as a last resort, after all other options have been exhausted – i.e. if death is imminent. Hyperventilation causes hypocapnia, which in turn causes cerebral vasoconstriction and thus decreased cerebral bloodflow. The end result of this is decreased ICP, however at the cost of possibly aggravating secondary brain injury due to hypoxia associated with hypoperfusion (Stocchetti et al., 2005; Smith, 2005)

Hypoxia is also to be avoided in head injury patients, as a decreased blood oxygen saturation leads to acidosis, which results in vasodilation. Vasodilation results in an increased ICP, further compounding brain injury (Shah & Kelly, 1999)

As per the Monro-Kellie Doctrine, ICP is directly related to the volume of contents within the cranial vault.

v.intracranial vault = [v.brain + v.csf + v.blood]

Therefore, to decrease ICP, blood, CSF or cerebral mass must be decreased. As the volume of CSF and amount of cerebral matter remains static, the alteration in blood flow is the main component that is adjusted (through vasoconstriction and vasodilation) to adjust ICP. (Mokri, 2001)

The use of cervical collars in patients with severe head injuries – helpful or harmful?

Any patient with a significant mechanism of injury is treated for suspected spinal injury as per protocol in many jurisdictions. Recent studies have shown however that the application of rigid cervical collars can result in a marked increase in ICP, with increases of up to 12mmHg noted in some studies (Hunt et al, 2001)

The very nature of rigid cervical collars means they are applied firmly, and thus can impede venous drainage from the cranial vault. (Craig & Nielsen, 1991). They can also act as a nociceptive stimulus, further increasing ICP.

There are limited options for replacing rigid cervical collars in the prehospital setting. The risk of spinal injury with severe head injuries is too great to recommend non-application of rigid cervical collars. As per Hunt et al. (2001) the recommendation is to x-ray and examine the patient’s cervical spine as soon as practicable on admission to the ED, and remove the rigid collar if possible at the earliest opportunity. If this is not possible, then replacement with a soft collar or other forms of spinal immobilisation is recommended.

Primary v Secondary Brain Injury

Primary Brain Injury

This results from what happens to the brain at the time of initial injury.

Secondary Brain Injury

This results from the biological, physiological and biochemical effects that occur as a result of primary injury. Examples of this include hypoxia, necrosis, cerebral oedema, inflammation, and ischaemia. (AAOS, 2005)

Helmet efficiency in reducing incidence of head injuries sustained whilst cycling

According to Henderson (1995) “Wearing a helmet substantially reduces the risk of head injury to a cyclist in a crash. This has been shown by a raft of strong evidence generated by epidemiological and biomechanical research, and cited in the present report.”

In a study carried out by Maimaris et al. (1992) a head injury was sustained by four out of 114 (4 per cent) of helmet wearers, compared with 100 out of 928 (11 per cent) of non-helmet wearers. The risk reduction in wearing a helmet was concluded to by over 60%. They also found that all the patients who had sustained traumatic brain injuries, and two fatalities which resulted from head injuries had not been wearing helmets at time of injury.

Whilst not a legal requirement, several studies including those cited above have shown that wearing a helmet whilst cycling significantly reduces the incidence of head injuries sustained in the event of a collision or fall.

References (non-PubMed)

AAOS (2005) Emergency Care and Transportation of the Sick and Injured 9th Edition. Massachusetts: Jones & Bartlett

Elling B, Caroline N, Smith M (2007) Nancy Caroline’s Emergency Care in the Streets, 6th Edition (UK Edition). London: LWW

Gausche-Hill, M (2004) Pediatric Airway Management for the Prehospital Professional. Massachusetts: Jones & Bartlett

Henderson M (1995) The Effectiveness of Bicycle Helmets: A Review. Summary for the Motor Accidents Authority of New South Wales, Australia. Bicycle Helmet Safety Institute.

JRCALC (2006) UK Ambulance Service Clinical Practice Guidelines 2006. JRCALC

Shah S, Kelly K (1999) Emergency Neurology. Cambridge: Cambridge University Press

Smith S (2005) ICP & Head Trauma. Presentation to US Army Medical Corps Staff, June 2005. Unpublished

References

 
 
 
 
 
 
 
 
 
 
 
 

2.

Bernard SA1, Smith K, Porter R, Jones C, Gailey A, Cresswell B, Cudini D, Hill S, Moore B, St Clair T. Paramedic rapid sequence intubation in patients with non-traumatic coma. Emerg Med J. 2014 Jan 28. PMID: 24473409.

Pre-hospital intubation by paramedics is widely used in comatose patients prior to transportation to hospital, but the optimal technique for intubation is uncertain. One approach is paramedic rapid sequence intubation (RSI), which may improve outcomes in adult patients with traumatic brain injury. H […]

4.

Craig GR1, Nielsen MS. Rigid cervical collars and intracranial pressure. Intensive Care Med. 1991;17(8):504-5. PMID: 1797898.

The use of a rigid cervical collar is widely recommended for patients with impaired consciousness following a head injury. This report suggests that such collars may cause significant increases in intracranial pressure in some patients and that this should be borne in mind when they are used. […]

6.

Hunt K1, Hallworth S, Smith M. The effects of rigid collar placement on intracranial and cerebral perfusion pressures. Anaesthesia. 2001 Jun;56(6):511-3. PMID: 11412154.

Rigid collars are routinely used to immobilise the cervical spine during early management of trauma victims until spinal injury is excluded. Spinal injuries commonly coexist in patients with severe head injury, and there is still uncertainty as to whether application of a rigid collar may adversely […]

8.

Mokri B. The Monro-Kellie hypothesis: applications in CSF volume depletion. Neurology. 2001 Jun 26;56(12):1746-8. PMID: 11425944.

More than two centuries ago, Alexander Monro applied some of the principles of physics to the intracranial contents and for the first time hypothesized that the blood circulating in the cranium was of constant volume at all times. This hypothesis was supported by experiments by Kellie. In its origin […]

10.

Sloane C1, Vilke GM, Chan TC, Hayden SR, Hoyt DB, Rosen P. Rapid sequence intubation in the field versus hospital in trauma patients. J Emerg Med. 2000 Oct;19(3):259-64. PMID: 11033272.

We conducted a retrospective review of all adult trauma patients who underwent prehospital field rapid sequence intubation (RSI) by aeromedical crews from 1988 through 1995 and compared them to all trauma patients who arrived by ground transportation and underwent RSI in the trauma suite from 1992 t […]

11.

Stocchetti N1, Maas AI, Chieregato A, van der Plas AA. Hyperventilation in head injury: a review. Chest. 2005 May;127(5):1812-27. PMID: 15888864.

The aim of this review was to consider the effects of induced hypocapnia both on systemic physiology and on the physiology of the intracranial system. Hyperventilation lowers intracranial pressure (ICP) by the induction of cerebral vasoconstriction with a subsequent decrease in cerebral blood volume […]

12.

Wang HE1, Yealy DM. Out-of-hospital endotracheal intubation: where are we? Ann Emerg Med. 2006 Jun;47(6):532-41. PMID: 16713780.

While remaining prominent in paramedic care and beneficial to some patients, out-of-hospital endotracheal intubation has not clearly improved survival or reduced morbidity from critical illness or injury when studied more broadly. Recent studies identify equivocal or unfavorable clinical effects, ad […]

Tags: case study, CVA, neurology, stroke, trauma

1. Stroke Unit Trialists' Collaboration. Organised inpatient (stroke unit) care for stroke. Cochrane Database Syst Rev. 2002 CD000197. [PubMed]

2. Sulter G, Elting JW, Langedijk M, Maurits NM, De Keyser J. Admitting acute ischemic stroke patients to a stroke care monitoring unit versus a conventional stroke unit: A randomized pilot study. Stroke. 2003;34:101–4.[PubMed]

3. Cavallini A, Micieli G, Marcheselli S, Quaglini S. Role of monitoring in management of acute ischemic stroke patients. Stroke. 2003;34:2599–603.[PubMed]

4. Leira R, Blanco M, Rodriguez-Yanez M, Flores J, Garcia-Garcia J. Non-pharmacological neuroprotection: Role of emergency stroke management. Cerebrovasc Dis. 2006;21:89–98.[PubMed]

5. Dawson SL, Blake MJ, Panerai RB, Potter JF. Dynamic but not static cerebral autoregulation is impaired in acute ischemic stroke. Cerebrovasc Dis. 2000;10:126–32.[PubMed]

6. Sugimori H, Ibayashi S, Fujii K, Yao H, Sadoshima S, Fujishima M. Brain infarction developed in hypertensive and normotensive patients during hospitalization--hemodynamic factors. Angiology. 1995;46:473–80.[PubMed]

7. Morfis L, Schwartz RS, Poulos R, Howes LG. Blood pressure changes in acute cerebral infarction and hemorrhage. Stroke. 1997;28:1401–5.[PubMed]

8. Wallace JD, Levy LL. Blood pressure after stroke. JAMA. 1981;246:2177–80.[PubMed]

9. Britton M, Carlsson A, de Faire U. Blood pressure course in patients with acute stroke and matched controls. Stroke. 1986;17:861–4.[PubMed]

10. Wong AA, Davis JP, Schluter PJ, Henderson RD, O'Sullivan DJ, Read SJ. The time course and determinants of blood pressure within the first 48 h after ischemic stroke. Cerebrovasc Dis. 2007;24:426–33.[PubMed]

11. Aslanyan S, Fazekas F, Weir CJ, Horner S, Lees KR. Effect of blood pressure during the acute period of ischemic stroke on stroke outcome: A tertiary analysis of the GAIN International Trial. Stroke. 2003;34:2420–5.[PubMed]

12. Leonardi-Bee J, Bath PM, Phillips S, Sandercock P. Blood pressure and clinical outcome in the International Stroke Trial. Stroke. 2002;33:1315–20.[PubMed]

13. Carlberg B, Asplund K, Hagg E. Factors influencing admission blood pressure levels in patients with acute stroke. Stroke. 1991;22:527–30.[PubMed]

14. Morfis L, Schwartz R, Lykos D, Zagami A, Pryor D, Howes LG. 24 hour ambulatory blood pressure profiles in the acute phase of stroke. Clin Exp Pharmacol Physiol. 1995;22:775–7.[PubMed]

15. Ahmed N, de la Torre B, Wahlgren NG. Salivary cortisol, a biological marker of stress, is positively associated with 24-hour systolic blood pressure in patients with acute ischemic stroke. Cerebrovasc Dis. 2004;18:206–13.[PubMed]

16. Fujishima S, Abe I, Okada Y, Saku Y, Sadoshima S, Fujishima M. Serial changes in blood pressure and neurohormone levels after the onset of lacunar stroke. Angiology. 1996;47:579–87.[PubMed]

17. Christensen H, Boysen G, Johannesen HH. Serum-cortisol reflects severity and mortality in acute stroke. J Neurol Sci. 2004;217:175–80.[PubMed]

18. Di Napoli M, Papa F. Association between blood pressure and C-reactive protein levels in acute ischemic stroke. Hypertension. 2003;42:1117–23.[PubMed]

19. Johansson A, Olsson T, Carlberg B, Karlsson K, Fagerlund M. Hypercortisolism after stroke--partly cytokine-mediated? J Neurol Sci. 1997;147:43–7.[PubMed]

20. Wityk RJ. The management of blood pressure after stroke. Neurologist. 2007;13:171–81.[PubMed]

21. Marcheselli S, Cavallini A, Tosi P, Quaglini S, Micieli G. Impaired blood pressure increase in acute cardioembolic stroke. J Hypertens. 2006;24:1849–56.[PubMed]

22. Christensen H, Boysen G. Blood glucose increases early after stroke onset: A study on serial measurements of blood glucose in acute stroke. Eur J Neurol. 2002;9:297–301.[PubMed]

23. Vemmos KN, Tsivgoulis G, Spengos K, Zakopoulos N, Synetos A, Manios E, et al. U-shaped relationship between mortality and admission blood pressure in patients with acute stroke. J Intern Med. 2004;255:257–65.[PubMed]

24. Vemmos KN, Spengos K, Tsivgoulis G, Zakopoulos N, Manios E, Kotsis V, et al. Factors influencing acute blood pressure values in stroke subtypes. J Hum Hypertens. 2004;18:253–9.[PubMed]

25. Gerraty RP, Parsons MW, Barber PA, Darby DG, Desmond PM, Tress BM, et al. Examining the lacunar hypothesis with diffusion and perfusion magnetic resonance imaging. Stroke. 2002;33:2019–24.[PubMed]

26. Yong M, Diener HC, Kaste M, Mau J. Characteristics of blood pressure profiles as predictors of long-term outcome after acute ischemic stroke. Stroke. 2005;36:2619–25.[PubMed]

27. Aslanyan S, Weir CJ, Lees KR. Elevated pulse pressure during the acute period of ischemic stroke is associated with poor stroke outcome. Stroke. 2004;35:e153–5.[PubMed]

28. Stead LG, Gilmore RM, Vedula KC, Weaver AL, Decker WW, Brown RD., Jr Impact of acute blood pressure variability on ischemic stroke outcome. Neurology. 2006;66:1878–81.[PubMed]

29. Dawson SL, Manktelow BN, Robinson TG, Panerai RB, Potter JF. Which parameters of beat-to-beat blood pressure and variability best predict early outcome after acute ischemic stroke? Stroke. 2000;31:463–8.[PubMed]

30. Pandian JD, Wong AA, Lincoln DJ, Davis JP, Henderson RD, O' Sullivan JD, et al. Circadian blood pressure variation after acute stroke. J Clin Neurosci. 2006;13:558–62.

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