Tag Archives: resuscitation

Acute Med, All Updates, PHARM, Resus, Ultrasound

Prehospital echo predicts arrest outcome

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In hospital, the detection of cardiac standstill with ultrasound predicts a fatal outcome from cardiac arrest with a high degree of accuracy. A similar finding has been made in the prehospital setting. Interestingly, it was a better predictor than other commonly recognised factors associated with outcome: the presence of asystole, down time, bystander CPR, or end-tidal CO2 levels.


Introduction. The prognostic value of emergency echocardiography (EE) in the management of cardiac arrest patients has previously been studied in an in-hospital setting. These studies mainly included patients who underwent cardiopulmonary resuscitation (CPR) by emergency medicine technicians at the scene and who arrived at the emergency department (ED) still in a state of cardiac arrest. In most European countries, cardiac arrest patients are normally treated by physician-staffed emergency medical services (EMS) teams on scene. Transportation to the ED while undergoing CPR is uncommon. Objective. To evaluate the ability of EE to predict outcome in cardiac arrest patients when it is performed by ultrasound-inexperienced emergency physicians on scene.

Methods. We performed a prospective, observational study of nonconsecutive, nontrauma, adult cardiac arrest patients who were treated by physician-staffed urban EMS teams on scene. Participating emergency physicians (EPs) received a two-hour course in EE during CPR. After initial procedures were accomplished, EE was performed during a rhythm and pulse check. A single subxiphoid, four-chamber view was required for study enrollment. We defined sonographic evidence of cardiac kinetic activity as any detected motion of the myocardium, ranging from visible ventricular fibrillation to coordinated ventricular contractions. The CPR had to be continued for at least 15 minutes after the initial echocardiography. No clinical decisions were made based on the results of EE.

Results. Forty-two patients were enrolled in the study. The heart could be visualized successfully in all patients. Five (11.9%) patients survived to hospital admission. Of the 32 patients who had cardiac standstill on initial EE, only one (3.1%) survived to hospital admission, whereas four out of 10 (40%) patients with cardiac movement on initial EE survived to hospital admission (p = 0.008). Neither asystole on initial electrocardiogram nor peak capnography value, age, bystander CPR, or downtime was a significant predictor of survival. Only cardiac movement was associated with survival, and cardiac standstill at any time during CPR resulted in a positive predictive value of 97.1% for death at the scene.

Conclusion. Our results support the idea of focused echocardiography as an additional criterion in the evaluation of outcome in CPR patients and demonstrate its feasibility in the prehospital setting.

Cardiac Movement Identified on Prehospital Echocardiography Predicts Outcome
Prehosp Emerg Care. 2012 Jan 11. [Epub ahead of print]

All Updates, ICU, PHARM, Resus, Trauma

FIRST: Fluids in Resuscitation of Severe Trauma

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This is the first randomized, controlled, double-blind study comparing crystalloids with isotonic colloids in trauma. 0.9% saline was compared with hydroxyethyl starch, HES 130/0.4, as a resuscitation fluid in pre-defined subgroups of penetrating and blunt trauma. While a primary outcome measure of gastrointestinal recovery might not seem an obvious choice to some of us, previous research has indicated this to be an issue with crystalloid and the authors clearly defined this as a predefined outcome when registering the trial here.

I don't have any pictures of colloids. Here's where I work.

Colloids tend to require smaller volumes than crystalloid to achieve the same degree of plasma expansion. An interesting finding in this study is that the volume of saline administered was 1.5 times that of hydroxyethyl starch – a very similar ratio to that seen in the SAFE study which compared saline with 4% albumin in intensive care patients.
The authors assert: “..the better lactate clearance in the P-HES group indicated superior tissue resuscitation with the colloid.” There are a number of reasons why this might be a bit of stretch, including the use of epinephrine in some patients which is known to be a cause of hyperlactataemia.
This is a small study whose conclusions should be treated with caution, but which provides an important contribution to the pool of fluid resuscitation literature. If you have full text access to the British Journal of Anaesthesia, the letters pages provide excellent critiques and responses regarding potential flaws in this paper. Nevertheless, it’s one to know about – I’m sure the FIRST trial is going to be quoted for some time to come, including, I suspect, by the manufacturers of certain colloids.


Background The role of fluids in trauma resuscitation is controversial. We compared resuscitation with 0.9% saline vs hydroxyethyl starch, HES 130/0.4, in severe trauma with respect to resuscitation, fluid volume, gastrointestinal recovery, renal function, and blood product requirements.

Methods Randomized, controlled, double-blind study of severely injured patients requiring>3 litres of fluid resuscitation. Blunt and penetrating trauma were randomized separately. Patients were followed up for 30 days.

Results A total of 115 patients were randomized; of which, 109 were studied. For patients with penetrating trauma (n=67), the mean (sd) fluid requirements were 5.1 (2.7) litres in the HES group and 7.4 (4.3) litres in the saline group (P<0.001). In blunt trauma (n=42), there was no difference in study fluid requirements, but the HES group required significantly more blood products [packed red blood cell volumes 2943 (1628) vs 1473 (1071) ml, P=0.005] and was more severely injured than the saline group (median injury severity score 29.5 vs 18; P=0.01). Haemodynamic data were similar, but, in the penetrating group, plasma lactate concentrations were lower over the first 4 h (P=0.029) and on day 1 with HES than with saline [2.1 (1.4) vs 3.2 (2.2) mmol litre−1; P=0.017]. There was no difference between any groups in time to recovery of bowel function or mortality. In penetrating trauma, renal injury occurred more frequently in the saline group than the HES group (16% vs 0%; P=0.018). In penetrating trauma, maximum sequential organ function scores were lower with HES than with saline (median 2.4 vs 4.5, P=0.012). No differences were seen in safety measures in the blunt trauma patients.
Conclusions In penetrating trauma, HES provided significantly better lactate clearance and less renal injury than saline. No firm conclusions could be drawn for blunt trauma.

Resuscitation with hydroxyethyl starch improves renal function and lactate clearance in penetrating trauma in a randomized controlled study: the FIRST trial (Fluids in Resuscitation of Severe Trauma)

Br J Anaesth. 2011 Nov;107(5):693-702

All Updates, ICU, Kids, PHARM, Resus

A big brain saves a little one

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Something I’ve been teaching for years – but never actually done – has been described in a case report from Oman.
A 2 year old child suffered a respiratory arrest due to an inhaled foreign body, which led to a bradyasystolic cardiac arrest. She was intubated by the resuscitation team who could not achieve any ventilation through the tube. The tube was removed and reinserted by an ‘expert’ (there is no mention of capnometry, for what it’s worth) and the same problem persisted.
The life-saving manouevre was to insert the tracheal tube further down into the right main bronchus and then withdraw to the trachea. This forced the obstructing object distally so that one-lung ventilation was then possible, resulting in return of spontaneous circulation and oxygen saturations in the mid-80’s. The object – a broken piece of plastic – was removed bronchoscopically and happily the child made an uneventful recovery.
Is this technique in your list of life-saving tricks? Hopefully, it is now.
A child is alive because a doctor was able to ‘think outside the guidelines’ in an incredibly high pressure situation. Rigid adherence to ACLS procedures here would have been futile. The guidelines save lives, but a few more can be saved when care can be individualised to the clinical situation by a thinking clinician.
Well done Dr Mishra and colleagues.

Sudden near-fatal tracheal aspiration of an undiagnosed nasal foreign body in a small child
Emerg Med Australas. 2011 Dec;23(6):776-8
[And here’s something else to consider if you have no airway equipment with you and your basic choking algorithm isn’t working]

All Updates, ICU, PHARM, Resus

Emergency percutaneous airway

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An excellent thorough review of emergency needle and surgical cricothyroidotomy – collectively described as ’emergency percutaneous airway’ – reveals a number of pearls.
Regarding anatomy:

  • The cricothyroid menbrane has an average height of 10 mm and a width of 11 mm
  • Transverse incision in the lower half of the cricothyroid membrane is recommended to avoid the cricothyroid arteries and the vocal cords

Regarding oxygenation / ventilation via a cricothyroid needle:

  • High pressure source ventilation via a needle (eg. by Sanders injector or Manujet) may cause laryngospasm, so a neuromuscular blocking agent should be considered
  • Barotrauma may result from an obstructed upper airway, so efforts should be made to maintain upper airway patency where possible (eg. with a supraglottic airway)
  • A device has been manufactured that provides suction-generated expiratory ventilation assistance (using oxygen flow and the Bernoulli principle) – the Ventrain
  • The Fourth National Audit Project reported a much lower success rate and described several complications of attempted re-oxygenation via a narrow-bore cricothyroidotomy
  • Where there is no kink-resistant cannula or suitable high-pressure source ventilation device readily available, it is probably safer to perform a wide-bore cannula puncture or surgical cricothyroidotomy.

Wide-bore cannula-over trocar devices:

  • Include the Quicktrach II and Portex cricothyroidotomy kit
  • Sometimes require considerable force to push the device through the cricothyroid membrane, risking compression of the airway and damage or perforation of the posterior tracheal wall.

Seldinger cricothyroidotomy kits:

  • Separate the puncture and dilatation steps, minimising the risk of trauma
  • Include the Melker emergency cricothyroidotomy set, available in sizes 3.0–6.0 mm ID
  • Tend to be preferred by anaesthetists over the surgical and wide-bore cannula-over-trocar techniques
  • Seldinger technique in human cadavers and manikin studies by those well trained, inexperienced operators have low success rates and a long performance time

What about after?

  • High-pressure source ventilation may aid subsequent intubation by direct laryngoscopy as bubbles may be seen emerging from the glottis.
  • The Seldinger technique has been recommended to convert a narrow-bore cannula into a cuffed wide-bore cricothyroidotomy
  • While conversion of cricothyroidotomy to tracheostomy within 72 h has been advocated because of the increased risk of developing subglottic stenosis with prolonged intubation through the cricothyroid membrane, this risk may be much lower than previously believed
  • The risk of conversion, although less well examined, may also be appreciable

Which technique is best?

  • The recent NAP4 audit reported a success rate of only 37% for narrow-bore cannula-over-needle cricothyroidotomy, 57% for wide-bore cannula techniques and 100% for surgical cricothyroidotomy
  • Simulation studies show conflicting results about whether seldinger or surgical technique is faster.
  • Reported success rates of the different techniques (in simulations) also vary widely and range for surgical cricothyroidotomy from 55% to 100%, for wide-bore cannula-over-trocar from 30% to 100%, and for Seldinger technique from 60% to 100%.

The one area of some consensus is that conventional (low-pressure source) ventilation should not be used with a narrow-bore cannula; a high-pressure oxygen source and a secure pathway for the egress of gas are both mandatory to achieve adequate ventilation.
Complications may be related to technique:

  • Complications of narrow-bore cannula techniques are ventilation-related and include barotrauma, subcutaneous emphysema, pneumothorax, pneumomediastinum and circulatory arrest due to impaired venous return; Cannula obstruction due to kinking also occurs.
  • Seldinger technique may be complicated by kinking of the guidewire, which increases the risk of tube misplacement
  • Bleeding and laryngeal fracture may complicate the surgical method, and long-term complications include subglottic stenosis, scarring and voice changes.

Equipment and strategies for emergency tracheal access in the adult patient
Anaesthesia. 2011 Dec;66 Suppl 2:65-80

Acute Med, All Updates, Guidelines, ICU, Kids, PHARM, Resus

Two new anaphylaxis guidelines

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Many local and national guidelines for the management of anaphylaxis exist, but did you know there was a World Allergy Organization, and it has a very detailed guideline on this important life threatening condition?

Some interesting snippets from the guideline are included here

Anaphylaxis and cardiac disease

  • Anaphylaxis can precipitate acute myocardial infarction in susceptible individuals: in patients with ischemic heart disease, the number and density of cardiac mast cells is increased, including in the atherosclerotic plaques. Mediators released during anaphylaxis contribute to vasoconstriction and coronary artery spasm.
  • Epinephrine is not contraindicated in the treatment of anaphylaxis in patients with known or suspected cardiovascular disease, or in middle-aged or elderly patients without any history of coronary artery disease who are at increased risk of ACS only because of their age. Through its beta-1 adrenergic effects, epinephrine actually increases coronary artery blood flow because of an increase in myocardial contractility and in the duration of diastole relative to systole.
  • Glucagon has noncatecholamine-dependent inotropic and chronotropic cardiac effects, and is sometimes needed in patients taking a beta-adrenergic blocker who have hypotension and bradycardia and who do not respond optimally to epinephrine.
  • Anticholinergic agents are sometimes needed in beta-blocked patients, for example, atropine in those with persistent bradycardia or ipratropium in those with epinephrine-resistant bronchospasm.

How quickly can untreated anaphylaxis kill you?

Studies show median times to cardiorespiratory arrest after exposure to the offending stimulus were 5 minutes after administration of contrast media or drugs, 15 minutes after an insect sting, and 30 minutes after food ingestion.

What about confirming the diagnosis with serum tryptase measurements?

  • Blood samples for measurement of tryptase levels are optimally obtained 15 minutes to 3 hours after symptom onset.
  • Blood samples for measurement of histamine levels are optimally obtained 15–60 minutes after symptom onset. These tests are not specific for anaphylaxis.
  • Increased serum tryptase levels are often found in patients with anaphylaxis from insect stings or injected medications, and in those who are hypotensive
  • However, levels are often within normal limits in patients with anaphylaxis triggered by food and in those who are normotensive
  • Serial measurement of tryptase levels during an anaphylactic episode, and measurement of a baseline level after recovery are reported to be more useful than measurement at only one point in time.
  • Normal levels of either tryptase or histamine do not rule out the clinical diagnosis of anaphylaxis


How does epinephrine help?

  • Epinephrine is life-saving because of its alpha-1 adrenergic vasoconstrictor effects in most body organ systems (skeletal muscle is an important exception) and its ability to prevent and relieve airway obstruction caused by mucosal edema, and to prevent and relieve hypotension and shock.
  • Other relevant properties in anaphylaxis include its beta-1 adrenergic agonist inotropic and chronotropic properties leading to an increase in the force and rate of cardiac contractions, and its beta-2 adrenergic agonist properties such as decreased mediator release, bronchodilation and relief of urticaria
  • Epinephrine in a dose of 0.01 mg/kg of a 1:1,000 (1 mg/mL) solution injected promptly by the intramuscular route is effective and safe in the initial treatment of anaphylaxis. In other anaphylaxis scenarios, this low first-aid dose is unlikely to be effective. For example, if shock is imminent or has already developed, epinephrine needs to be given by slow intravenous infusion, ideally with the dose titrated according to noninvasive continuous cardiac monitoring.

What is the empty ventricle syndrome?

  • Patients with anaphylaxis should not suddenly sit, stand, or be placed in the upright position.
  • Instead, they should be placed on the back with their lower extremities elevated or, if they are experiencing respiratory distress or vomiting, they should be placed in a position of comfort with their lower extremities elevated.
  • This accomplishes 2 therapeutic goals: 1) preservation of fluid in the circulation (the central vascular compartment), an important step in managing distributive shock; and 2) prevention of the empty vena cava/empty ventricle syndrome, which can occur within seconds when patients with anaphylaxis suddenly assume or are placed in an upright position.
  • Patients with this syndrome are at high risk for sudden death. They are unlikely to respond to epinephrine regardless of route of administration, because it does not reach the heart and therefore cannot be circulated throughout the body

Should we give antihistamines, beta 2 agonists, and steroids?

The evidence base for use of these second line medications in the initial management of anaphylaxis, is extrapolated mainly from their use in treatment of other diseases such as urticaria (antihistamines) or acute asthma (beta-2 adrenergic agonists and glucocorticoids). Concerns have been raised that administering one or more second-line medications potentially delays prompt injection of epinephrine, the first-line treatment


Is ‘biphasic anaphylaxis’ a real phenomenon we should be concerned about?

  • Biphasic anaphylaxis occurs when symptoms recur within 1–72 hours (usually within 8–10 hours) after the initial symptoms have resolved, despite no further exposure to the trigger.
  • It occurs in up to 23% of adults and up to 11% of children.
  • After apparent resolution of symptoms, duration of monitoring in a medically supervised setting should be individualized. For example, patients with moderate respiratory or cardiovascular compromise should be monitored for at least 4 hours, and if indicated, for 8–10 hours or longer.
  • Protracted uniphasic anaphylaxis is uncommon, but can last for days.

World Allergy Organization Guidelines for the Assessment and Management of Anaphylaxis
World Allergy Organization Journal 2011;4(2):13-37 Full Text
[EXPAND click for abstract]

The illustrated World Allergy Organization (WAO) Anaphylaxis Guidelines were created in response to absence of global guidelines for anaphylaxis. Uniquely, before they were developed, lack of worldwide availability of essentials for the diagnosis and treatment of anaphylaxis was documented. They incorporate contributions from more than 100 allergy/immunology specialists on 6 continents. Recommendations are based on the best evidence available, supported by references published to the end of December 2010. The Guidelines review patient risk factors for severe or fatal anaphylaxis, co-factors that amplify anaphylaxis, and anaphylaxis in vulnerable patients, including pregnant women, infants, the elderly, and those with cardiovascular disease. They focus on the supreme importance of making a prompt clinical diagnosis and on the basic initial treatment that is urgently needed and should be possible even in a low resource environment. This involves having a written emergency protocol and rehearsing it regularly; then, as soon as anaphylaxis is diagnosed, promptly and simultaneously calling for help, injecting epinephrine (adrenaline) intramuscularly, and placing the patient on the back or in a position of comfort with the lower extremities elevated. When indicated, additional critically important steps include administering supplemental oxygen and maintaining the airway, establishing intravenous access and giving fluid resuscitation, and initiating cardiopulmonary resuscitation with continuous chest compressions. Vital signs and cardiorespiratory status should be monitored frequently and regularly (preferably, continuously). The Guidelines briefly review management of anaphylaxis refractory to basic initial treatment. They also emphasize preparation of the patient for self-treatment of anaphylaxis recurrences in the community, confirmation of anaphylaxis triggers, and prevention of recurrences through trigger avoidance and immunomodulation. Novel strategies for dissemination and implementation are summarized. A global agenda for anaphylaxis research is proposed.

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This month has also seen the publication guidelines from the UK’s National Institute for Health & Clinical Excellence, entitled ‘Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode’
Their guideline summary is as follows:

After a suspected anaphylactic reaction in adults or young people aged 16 years or older, take timed blood samples for mast cell tryptase testing as follows:

  • a sample as soon as possible after emergency treatment has started
  • a second sample ideally within 1–2 hours (but no later than 4 hours) from the onset of symptoms.

After a suspected anaphylactic reaction in children younger than 16 years, consider taking blood samples for mast cell tryptase testing as follows if the cause is thought to be venom-related, drug-related or idiopathic:

  • a sample as soon as possible after emergency treatment has started
  • a second sample ideally within 1–2 hours (but no later than 4 hours) from the onset of symptoms.

Patients who have had emergency treatment for suspected anaphylaxis should be observed for 6–12 hours from the onset of symptoms, depending on their response to emergency treatment
After emergency treatment for suspected anaphylaxis, offer people a referral to a specialist allergy service (age-appropriate where possible) consisting of healthcare professionals with the skills and competencies necessary to accurately investigate, diagnose, monitor and provide ongoing management of, and patient education about, suspected anaphylaxis.
After emergency treatment for suspected anaphylaxis, offer people (or, as appropriate, their parent and/or carer) an appropriate adrenaline injector as an interim measure before the specialist allergy service appointment.
Before discharge a healthcare professional with the appropriate skills and competencies should offer people (or, as appropriate, their parent and/or carer) the following:

  • information about anaphylaxis, including the signs and symptoms of an anaphylactic reaction
  • information about the risk of a biphasic reaction
  • information on what to do if an anaphylactic reaction occurs (use the adrenaline injector and call emergency services)

Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode
CG134 Anaphylaxis: NICE guideline

Acute Med, All Updates, ICU, PHARM, Resus

Pre-hospital hypertonic saline during ACLS

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A newly published study examines pre-hospital hypertonic saline during CPR. A randomised trial compared 7.2% hypertonic saline / hydroxyethyl starch with hydroxyethyl starch alone in over 200 adult patients with non-traumatic out-of-hospital cardiac arrest. The volume infused was 2 ml /kg over 10 mins. All patients were resuscitated by the physicians of the Emergency Medical System (EMS) in Bonn, Germany.
There were no differences in survival to admission or discharge. There was a barely statistically significant increase in those survivors with higher cerebral performance categories (1 or 2) in the hypertonic saline group, inviting further study. The study was conducted from 2001 to 2004 (according to the 2000 CPR-Guidelines), so took an interestingly long time to see print.
Randomised study of hypertonic saline infusion during resuscitation from out-of-hospital cardiac arrest
Resuscitation. 2011 Sep 19. [Epub ahead of print]
[EXPAND Click to read abstract]


Aim of the study Animal models of hypertonic saline infusion during cardiopulmonary resuscitation (CPR) improve survival, as well as myocardial and cerebral perfusion during CPR. We studied the effect of hypertonic saline infusion during CPR (Guidelines 2000) on survival to hospital admission and hospital discharge, and neurological outcome on hospital discharge.

Methods The study was performed by the EMS of Bonn, Germany, with ethical committee approval. Study inclusion criteria were non-traumatic out-of-hospital cardiac arrest, aged 18–80 years, and given of adrenaline (epinephrine) during CPR. Patients were randomly infused 2 ml kg−1 HHS (7.2% NaCl with 6% hydroxyethyl starch 200,000/0.5 [HES]) or HES over 10 min.

Results 203 patients were randomised between May 2001 and June 2004. After HHS infusion, plasma sodium concentration increased significantly to 162 ± 36 mmol l−1 at 10 min after infusion and decreased to near normal (144 ± 6 mmol l−1) at hospital admission. Survival to hospital admission and hospital discharge was similar in both groups (50/100 HHS vs. 49/103 HES for hospital admission, 23/100 HHS vs. 22/103 HES for hospital discharge). There was a small improvement in neurological outcome in survivors on discharge (cerebral performance category 1 or 2) in the HHS group compared to the HES group (13/100 HHS vs. 5/100 HES, p < 0.05, odds-ratio 2.9, 95% confidence interval 1.004–8.5).
Conclusion Hypertonic saline infusion during CPR using Guidelines 2000 did not improve survival to hospital admission or hospital discharge. There was a small improvement with hypertonic saline in the secondary endpoint of neurological outcome on discharge in survivors. Further adequately powered studies using current guidelines are needed.

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Acute Med, All Updates, ICU, Resus

Cardiac arrest caused by subarachnoid haemorrhage

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We know that subarachnoid haemorrhage (SAH) can cause cardiac arrest. Some questions we may have about this are:

Questions

  • What proportion of out-of-hospital cardiac arrests (OOHCA) who achieve return of spontaneous circulation (ROSC) are caused by SAH?
  • What is the usual presenting arrest rhythm – VT/VF or non-shockable rhythms?
  • What is the outcome of these patients – do any survive?
  • Do they have other characteristic cardiac features, such as ECG or echo abnormalities?
  • Should we do a head CT on all survivors of out-of-hospital cardiac arrest of uncertain aetiology?

A recent Japanese article in Resuscitation1 is the third from that country to be published on the topic in three years, the other two2,3 coming from different centres and all demonstrating some consistent answers, as do papers published in recent years from Europe4 and North America5:

Answers

  • Rates of SAH in OOHCA patients who achieve ROSC and make it to CT range from 4-16% (even higher if other sources of intracranial haemorrhage are included).
  • Studies consistently demonstrate VT/VF to be very rare – PEA and asystole are by far the commonest presenting arrest rhythms.
  • Almost no patients with this presentation due to SAH survive to hospital discharge.
  • In the most recent study, all patients who survived long enough to get a 12 lead showed ST-T abnormalities and/or QT prolongation, although echocardiograms were mostly normal.
  • Rates of SAH in OOHCA patients who achieve ROSC seem to be sufficiently high to seriously consider head CT in these patients if there is no obvious alternate explanation for the arrest.

1. Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest
Resuscitation. 2011 Oct;82(10):1294-7
[EXPAND Abstract]


Background Subarachnoid haemorrhage (SAH) is known as one of the aetiologies of out-of-hospital cardiac arrest (OHCA). However, the mechanisms of circulatory collapse in these patients have remained unclear.

Methods and results We examined 244 consecutive OHCA patients transferred to our emergency department. Head computed tomography was performed on all patients and revealed the existence of SAH in 14 patients (5.9%, 10 females). Among these, sudden collapse was witnessed in 7 patients (50%). On their initial cardiac rhythm, all 14 patients showed asystole or pulseless electrical activity, but no ventricular fibrillation (VF). Return of spontaneous circulation (ROSC) was obtained in 10 of the 14 patients (14.9% of all ROSC patients) although all resuscitated patients died later. The ROSC rate in patients with SAH (71%) was significantly higher than that of patients with either other types of intracranial haemorrhage (25%, n = 2/8) or presumed cardiovascular aetiologies (22%, n = 23/101) (p < 0.01). On electrocardiograms, ST-T abnormalities and/or QT prolongation were found in all 10 resuscitated patients. Despite their electrocardiographic abnormalities, only 3 patients showed echocardiographic abnormalities.

Conclusions The frequency of SAH in patients with all causes of OHCA was about 6%, and in resuscitated patients was about 15%. The initial cardiac rhythm revealed no VF even though half had a witnessed arrest. A high ROSC rate was observed in patients with SAH, although none survived to hospital discharge.

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2. Assessing outcome of out-of-hospital cardiac arrest due to subarachnoid hemorrhage using brain CT during or immediately after resuscitation
Signa Vitae 2010; 5(2): 21 – 24 Full Text
[EXPAND Abstract]


Objectives. The clinical course and outcome of out-of-hospital cardiopulmonary arrest (OHCPA) due to subarachnoid hemorrhage (SAH) is unclear. The objective of this study is to clarify them.

Study design. Single- center, observational study. Setting. We usually perform a brain computed tomography (CT) in OHCPA patients who present without a clear etiology (42% of all OHCPA), such as trauma, to determine the cause of OHCPA and to guide treatment.

Patients. The study included OHCPA patients without a clear etiology, who were transferred to our center and who underwent a brain CT during resuscitation.

Methods of measurement. Patients’ records were reviewed; initial cardiac rhythm, existence of a witness and bystander cardiopulmonary resuscitation efforts (CPR) were compared with patients’ outcomes.

Results. Sixty-six patients were enrolled. 72.7% achieved return of spontaneous circulation (ROSC), 71.2% were admitted, 30.3% survived more than 7 days, and 9.1. survived-to-discharge. In 41 witnessed OHCPA, 87.8% obtained ROSC, 85.4% were admitted, and 14.6% survived-to-discharge. All survivors were witnessed. In 25 non-witnessed OHCPA, 48% obtained ROSC and were admitted, and no patients were discharged. Initial cardiac rhythm was ventricular fibrillation (VF), pulseless electrical activity (PEA) and asystole in 3.0%, 39.4%, and 47.0%. In 2 VF patients 50.0% survived-to- discharge, and there was no survivor with PEA or asystole.

Conclusion. This study shows a high rate of ROSC and admission in OHCPA patients with a SAH, and also reveals their very poor neurological outcome. We conclude that the detection of a SAH in OHCPA patients is important to determine the accurate frequency of SAH in this patient group and to guide appropriate treatment of all OHCPA patients.

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3. Subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest: A prospective computed tomography study
Resuscitation. 2009 Sep;80(9):977-80
[EXPAND Abstract]


Aim Aneurysmal subarachnoid haemorrhage (SAH) is a relatively common cause of out-of-hospital cardiac arrest (OHCA). Early identification of SAH-induced OHCA with the use of brain computed tomography (CT) scan obtained immediately after resuscitation may help emergency physicians make therapeutic decision as quickly as they can.

Methods During the 4-year observation period, brain CT scan was obtained prospectively in 142 witnessed non-traumatic OHCA survivors who remained haemodynamically stable after resuscitation. Demographics and clinical characteristics of SAH-induced OHCA survivors were compared with those with “negative” CT finding.

Results Brain CT scan was feasible with an average door-to-CT time of 40.0min. SAH was found in 16.2% of the 142 OHCA survivors. Compared with 116 survivors who were negative for SAH, SAH-induced OHCA survivors were significantly more likely to be female, to have experienced a sudden headache, and trended to have achieved return of spontaneous circulation (ROSC) prior to arrival in the emergency department less frequently. Ventricular fibrillation (VF) was significantly less likely to be seen in SAH-induced than SAH-negative OHCA (OR, 0.06; 95% CI, 0.01–0.46). Similarly, Cardiac Trop-T assay was significantly less likely to be positive in SAH-induced OHCA (OR, 0.08; 95% CI, 0.01–0.61).

Conclusion Aneurysmal SAH causes OHCA more frequently than had been believed. Immediate brain CT scan may particularly be useful in excluding SAH-induced OHCA from thrombolytic trial enrollment, for whom the use of thrombolytics is contraindicated. The low VF incidence suggests that VF by itself may not be a common cause of SAH-induced OHCA.

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4. Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest
Resuscitation. 2001 Oct;51(1):27-32
[EXPAND Abstract]


Objective: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest.

Design: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features.

Results: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome.

Conclusions: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.

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5. Cranial computed tomography in the resuscitated patient with cardiac arrest
Am J Emerg Med. 2009 Jan;27(1):63-7
[EXPAND Abstract]


Introduction The incidence of out-of-hospital and in-hospital cardiorespiratory arrest from all causes in the United States occurs not infrequently. Postresuscitation care should include the identification of the inciting arrest event as well as therapy tailored to support the patient and treat the primary cause of the decompensation. The application of one particular testing modality, cranial computed tomography (CT) of the head, has not yet been determined. We undertook an evaluation of the use of head CT in patients who were resuscitated from cardiac arrest.

Methods Prehospital (emergency medical services), ED, and hospital records were reviewed for patients of all ages with cardiorespiratory arrest over a 4-year period (July 1996-June 2000). Information regarding diagnosis, management, and outcome was recorded. The results of cranial CT, if performed, and any apparent resulting therapeutic changes were recorded. Patients with a known traumatic mechanism for the cardiorespiratory arrest were excluded.

Results A total of 454 patients (mean age 58.3 years with 60% male) with cardiorespiratory arrest were entered in the study with 98 (22%) individuals (mean age 58.5 years with 53% male) undergoing cranial CT. Arrest location was as follows: emergency medical services, 41 (42%); ED, 11 (11%); and hospital, 46 (47%). Seventy-eight (79%) patients demonstrated 111 CT abnormalities: edema, 35 (32%); atrophy, 24 (22%); extra-axial hemorrhage, 14 (13%); old infarct, 12 (11%); new infarct, 11 (10%); intraparenchymal hemorrhage, 6 (5%); skull fracture, 5 (4%); mass, 3 (2%); and foreign body, 1 (1%). Therapeutic and diagnostic alterations in care were made in 38 (39%) patients—35 abnormal and 3 normal CTs. The following alterations occurred: medication administration, 26; withdrawal of life support, 7; additional diagnostic study, 6; neurologic consultation, 6; and intracranial pressure monitoring. 4. No patient survived to discharge.

Conclusion In this subset of resuscitated patients with cardiac arrest, abnormalities on the head CT were not uncommon. Alterations in management did occur in those patients with abnormalities. The indications and impact of head CT in the population of resuscitated patients with cardiac arrest remain unknown, warranting further investigation.

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Acute Med, All Updates, Guidelines, ICU, Resus

Myoclonus no longer a show-stopper

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In comatose survivors of cardiac arrest, myoclonus is considered a grave prognostic sign. The American Academy of Neurology stated in 20061 that:
After cardiac arrest, the following clinical findings accurately predict poor outcome;

  • myoclonus status epilepticus within the first 24 hours in patients with primary circulatory arrest
  • absence of pupillary responses within days 1 to 3 after CPR
  • absent corneal reflexes within days 1 to 3 after CPR
  • and absent or extensor motor responses after 3 days.

However in the age of targeted temperature management the presence and/or timing of these signs needs to be re-evaluated. It has been suggested that therapeutic hypothermia and sedation required for induced cooling might delay recovery of motor reactions up to 5–6 days after cardiac arrest. Now a series of three survivors of cardiac arrest who had massive myoclonus in the first four hours after return of spontaneous circulation (ROSC) is reported2, all of whom were treated with TTM and experienced good neurologic outcomes.


Early myoclonus in comatose survivors of cardiac arrest, even when it is not myoclonic status epilepticus (MSE), is considered a sign of severe global brain ischemia and has been associated with high rates of mortality and poor neurologic outcomes. We report on three survivors of primary circulatory cardiac arrests who had good neurologic outcomes (two patients with a CPC score=1 and one patient with a CPC score=2) after mild therapeutic hypothermia, despite exhibiting massive myoclonus within the first four hours after return of spontaneous circulation. The concept that early myoclonus heralds a uniformly poor prognosis may need to be reconsidered in the era of post-cardiac arrest mild therapeutic hypothermia.

1. Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology
Neurology. 2006 Jul 25;67(2):203-10 Full Text
2. Neurologic Recovery After Therapeutic Hypothermia in Patients with Post-Cardiac Arrest Myoclonus
Resuscitation published on line 03 October 2011

Acute Med, All Updates, ICU, Kids, PHARM, Resus, Trauma

Easy rapid infusion set up

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Kapoor and Singh's system from the Open Access article - click for explanation

Here’s a nice and simple set up for rapid iv infusions using simple cheap equipment

Full details at the Scandinavian Journal Site
Novel rapid infusion device for patients in emergency situations
Scand J Trauma Resusc Emerg Med. 2011 Jun 10;19:35 (Free Full Text)

All Updates, PHARM, Resus, Trauma

Pre-hospital thoracotomy

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The London Helicopter Emergency Medical Service provides a physician / paramedic team to victims of trauma. One of the interventions performed by their physicians is pre-hospital resuscitative thoracotomy to patients with cardiac arrest due to penetrating thoracic trauma. They have published the outcomes from this procedure over a 15 year period which show an 18% survival to discharge rate, with a high rate of neurologically intact survivors1.
The article was submitted for publication on February 1, 2010, and in the discussion mentions a further two survivors from the procedure performed after conducting the study. It is likely therefore in the year and a half since submission still more patients have been saved. It will be interesting to read future reports from this team as the numbers accumulate; penetrating trauma missions are sadly increasing in frequency.
Having worked for these guys and performed this procedure in the field a few times myself, I can attest to the training and governance surrounding this system. The technique of clamshell thoracotomy is well described 2 and one I would recommend for the non-surgeon.

BACKGROUND: Prehospital cardiac arrest associated with trauma almost always results in death. A case of survival after prehospital thoracotomy was published in 1994 and several others have followed. This article describes the result of prehospital thoracotomy in a physician-led system for patients with stab wounds to the chest who suffered cardiac arrest on scene.
METHODS: A 15-year retrospective prehospital trauma database review identified victims of stab wounds to the chest who suffered cardiac arrest on scene and had thoracotomy performed according to local standard operating procedures.
RESULTS: Overall, 71 patients met inclusion criteria. Thirteen patients (18%) survived to hospital discharge. Neurologic outcome was good in 11 patients and poor in 2. Presenting cardiac rhythm was asystole in four patients, pulseless electrical activity in five, and unrecorded in the remaining four. All survivors had cardiac tamponade. The medical team was present at the time of cardiac arrest for six survivors (good neurologic outcome): arrived in the first 5 minutes after arrest in three patients (all good neurologic outcome), arrived 5 minutes to 10 minutes after arrest in two patients (one poor neurologic outcome), and in one patient (poor neurologic outcome) the period was unknown. Of the survivors, seven thoracotomies were performed by emergency physicians and six by anesthesiologists.
CONCLUSIONS: Prehospital thoracotomy is a well-established procedure in this physician-led prehospital service. Results from this and other similar systems suggest that when performed for the subgroup of patients described, significant numbers of survivors with good neurologic outcome can be expected.

1. 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
2. Emergency thoracotomy: “how to do it”
Emerg Med J. 2005 January; 22(1):22–24
Full text available here