RAPID SEQUENCE INTUBATION & PHARMACOLOGY

OVERVIEW
Rapid sequence induction intubation (RSI) has become the gold standard for management of the airway in trauma and critical illness. The technique of RSI has been demonstrated to increase success rates for intubation and reduce complications compared to pre-RSI techniques in a variety of emergent settings. (Kovacs, G., 2004) (Pearson, S., 2003) (Bair AE, 2002)
Rapid sequence intubation is not without risk, and the decision to employ RSI must be preceded by a risk-benefit analysis based upon proficiency with non-intubating airway maintenance skills, RSI pharmacology, and emergent intubation. Rapid sequence intubation can be divided into five phases: (1) preparation of patient and equipment; (2) preoxygenation; (3) premedication; (4) paralysis; and (5) placement of the tube.

Preparation

Although significant injury with physiologic instability may preclude prolonged preparation for RSI, all efforts should be made to allow for individualized assessment of comorbid conditions, airway status, predictors of difficult intubation, and anticipated pharmacologic regimen.

Preoxygenation

Although not originally considered an essential component of RSI, preoxygenation is mandatory if the oxygenation, ventilation, and hemodynamic status of the patient permit. The purpose of preoxygenation is to replace the nitrogen-dominant room air occupying the pulmonary functional residual capacity with a 100% oxygen reservoir, such that saturation of arterial hemoglobin (SaO2) is prolonged. This can be accomplished by gently assisting spontaneous respirations with 100% oxygen or simply allowing the patient to breathe 100% oxygen. An optimally preoxygenated healthy 70-kg adult will maintain SaO2 over 90% for approximately 8 minutes, an obese adult less than 3 minutes, and a 10-kg child less than 4 minutes. (Walls RM, 2004) More importantly, the desaturation from 90% SaO2 to 0% occurs much more rapidly than the fall from 100% to 90%. The approximate PaO2 at 90% SaO2 is 60 mmHg, and this decreases to 27 mmHg at an SaO2 of 50%. An injured patient with little compensatory reserve can decline from 90% to 0% literally in seconds.
It is imperative that providers caring for the injured be facile with all pharmacologic agents utilized for RSI, including both barbiturate and nonbarbiturate hypnotics, neuromuscular blocking agents, benzodiazepines, dissociative agents, and opiates. each patient should be individualized based upon type and mechanism of injury, comorbidities, and potential for adverse events. The majority of trauma patients, however, can be effectively intubated using a generalized pharmacologic regimen.

PREMEDICATION

Airway stimulation, including laryngoscopy and placement of an endotracheal tube, results in the pressor response, an intense autonomic sympathetic discharge producing tachycardia, hypertension, and increased intracranial pressure. (Reynolds SF, 2005) (Singh S, 2003)A common mnemonic for the preinduction regimen is LOAD, which includes Lidocaine, Opiates, Atropine, and a Defasciculating agent, although atropine is typically utilized in pediatric populations only.
Opioids. Depth of sedation may correlate with speed of intubation in RSI. (Sivilotti ML, 1998) The sedative and analgesic effects of opioids may provide benefit to the injured patient prior to induction. A commonly used opioid for RSI in the prehospital and emergency department setting is fentanyl, which at a dose of 5.0 mcg/kg has been shown to be hemodynamically neutral compared to midazolam and thiopental during RSI. (Sivilotti ML, 1998) Fentanyl effectively blunts airway reactivity (Tagaito Y, 1998) and confers the significant added benefit of analgesia in the injured patient.

Benzodiazepines

Benzodiazepines, a family of gamma aminobutyric acid (GABA) agonists, have been utilized in RSI for sedation. Midazolam is the most widely studied agent, having favorable pharmacokinetics for RSI, including rapid onset and short half-life. Advantages include hemodynamic neutrality and retrograde amnesia, although onset is slower than comparable agents and the intubation reflex is not attenuated. (Sivilotti ML, 1998) Therefore, it is less commonly used in RSI protocols than opioids.

Antiarrhythmics

Despite a great deal of controversy regarding the potential benefits of lidocaine during RSI, it is a preinduction agent common to RSI protocols (Robinson N, 2001) and is advocated in many emergency airway courses. Lidocaine has a number of theoretical beneficial preintubation effects, including abrogation of airway reactivity following placement of the endotracheal tube, the tachycardic response to intubation, and succinylcholine-induced myalgia and fasciculations. (Lev R, 1994), (Schreiber JW, 2005) The two primary potential benefits of use of lidocaine in RSI are to avoid reflex bronchospasm and increased intracranial pressure. The decision to use lidocaine in RSI becomes a potential benefit versus risk analysis. Although definitive data are lacking regarding effects on intracranial pressure, the potential benefits outweigh the negligible side effects of the RSI dose.

Defasciculation Paralytic Agents

Succinylcholine, the standard neuromuscular blocking agent utilized for RSI, produces significant myoclonal fasciculations, prompting a rise in intracranial pressure. Therefore, a defasciculating dose of a competitive neuromuscular blocking is administered during RSI. Common defasciculating agents include vecuronium and rocuronium, and, less commonly, pancuronium. Defasciculating doses are administered as 10% of the paralyzing dose, given 3 to 5 minutes prior to administration of succinylcholine. It is unusual for defasciculating doses of neuromuscular blockers to cause apnea. As patient weight is commonly an estimate during RSI following injury, however, preparations to assist with ventilation should be made.


Induction Agents

The purpose of induction agents in RSI is to induce rapid loss of consciousness to facilitate endotracheal intubation. The perfect induction agent would possess rapid onset and elimination, render the patient unconscious but also amnestic, possess analgesic properties, and have negligible side effects. In injured and critically ill patients, the ideal agent would produce little cardiovascular effects and maintain cerebral perfusion pressure. Regrettably, such an agent does not yet exist. Because many agents produce side effects, including myocardial depression with the potential for hypoperfusion, careful attention should be dedicated to the selection of individual agents, focusing on clinical presentation and patient specific characteristics.

Etomidate

Etomidate is a short acting carboxylated imidazole hypnotic agent frequently utilized for rapid sequence induction. Etomidate possesses ideal characteristics for urgent and emergent RSI in trauma patients, including rapid onset and clearance, reduction in cerebral metabolic rate, (Rodricks MB, 2000) and negligible effects on hemodynamics. This favorable pharmacokinetic profile has led to the widespread use of etomidate for RSI in patients with injury to the brain and hemodynamically labile patients. The most significant side effect of etomidate relates to adrenal insufficiency, as it produces a reversible blockade of adrenal 11-beta-hydroxylase. In patients at risk for adrenal insufficiency, including brain injured, mechanically ventilated, and septic populations, etomidate has been independently correlated with reductions in serum cortisol. (Jackson, 2005) (Malerba G, 2005) (Cohan P, 2005) The controversial question relates to whether transient adrenal suppression produces lasting effects on outcome. Further studies are warranted to determine the long-term safety of etomidate for RSI; however, given the multiple favorable characteristics of the drug, etomidate will remain the standard induction agent in most RSI protocols.

Propofol

Propofol is a nonbarbiturate hypnotic agent that rapidly induces deep sedation and significant relaxation of laryngeal musculature.28 When used for induction, propofol produces intubation conditions equal to thiopental (El-Orbany MI, 2003)and equal to or superior to etomidate. (Sivilotti ML F. M., 2003) Propofol should be used with caution in patients with injury to the brain or hemodynamically labile patients due to a consistent hypotensive effect and potential reduction of cerebral blood flow. Therefore, it should be considered an alternative agent in RSI.

Barbiturates

Thiopental is the most commonly used barbiturate for RSI. Like other induction agents used in RSI, thiopental has rapid onset and clearance. In the aeromedical setting, thiopental has been shown equally efficacious to etomidate as an adjunct to RSI. (Sonday CJ, 2005) Similarly, in an evaluation of 2380 RSI procedures, patients were more likely to be successfully intubated using thiopental or propofol as compared to etomidate or a benzodiazepine. (Sivilotti ML F. M., 2003) In addition, thiopental reduces cerebral oxygen consumption and exhibits anticonvulsant effects, rendering it useful in patients with injury to the brain. The significant limitation of thiopental use for RSI in trauma relates to inhibition of the sympathetic response of the central nervous system. Therefore, thiopental reduces myocardial contractility and systemic vascular resistance, and causes hypotension. Therefore, it is best reserved for patients who are euvolemic and normotensive, limiting its application in injured and critically ill patients.

Dissociative Agents

Ketamine, a rapid onset dissociative sedative and anesthetic agent, is frequently used for RSI in the pediatric population (Lee BS, 2001) and in adults with chronic obstructive pulmonary disease. (Marvez E, 2003)In addition to its sedative effects, ketamine exhibits the beneficial properties of potent analgesia and a partial amnesia. As a sympathomimetic agent, ketamine may induce tachycardia and increase blood pressure. In addition, ketamine induces cerebral vasodilatation, potentially exacerbating intracranial hypertension. Trauma patients with documented or potential injury to the brain should not undergo induction for RSI with ketamine. Given the sympathomimetic properties of ketamine, it is best reserved for patients with proven reactive airway disease and hypovolemia when injury to the brain has been definitively excluded.

Neuromuscular Blocking Agents

Pharmacologic paralysis represents an integral component of RSI, facilitating emergent intubation for more than three decades. (Thompson JD, 1982) (Brown EM, 1979) Paralysis of facial musculature facilitates optimal visualization during laryngoscopy, confers total control of the patient, and reduces complications during intubation. Prehospital neuromuscular blockade has been demonstrated to be safe (Zonies DH, 1998) (Rotondo MF, 1993), and to improve the success of intubation in injured patients undergoing RSI. (Bozeman WP, 2006) (Davis DP, 2003).

Succinylcholine

Succinylcholine, a depolarizing acetylcholine dimer, acts noncompetitively at the acetylcholine receptor in a biphasic manner to produce muscular paralysis at the motor end plate. Succinylcholine stimulates all muscarinic and nicotinic cholinergic receptors of both parasympathetic and sympathetic systems. Initial brief depolarization results in clinically notable muscular fasciculations, followed by sustained myocyte depolarization. Succinylcholine degradation is dependent on hydrolysis by pseudocholinesterase, and it is resistant to acetylcholinesterase. Due to rapid onset of action and a short half-life, succinylcholine remains the gold standard for RSI in patients not at risk for adverse events. The standardized dose of succinylcholine for RSI is 1.0 mg/kg, although the optimal dose for RSI is under evaluation. Recent data suggest that a smaller dose of 0.5-0.6 mg/kg is sufficient for RSI, (Naguib M, 2003) facilitating more rapid resumption of spontaneous respiration. Because complete paralysis represents an integral component of RSI, it is better to err toward complete paralysis when dosing in patients not at risk for adverse events. Intramuscular injection of succinylcholine has been described, although the required dose, 4 mg/kg is higher and onset is slower than with intravenous injection. (Schuh, 1982) Intramuscular injection should be absolutely reserved for the injured patient in whom a delay associated with intravenous or intraosseous access would be life-threatening.
A clear understanding of the potential adverse effects of succinylcholine is critical to its appropriate use in RSI. Contraindications are primarily related to existing hyperkalemia or conditions which accentuate the hyperkalemic effects of succinylcholine, as it normally produces a 0.5-1.0 mEq/L elevation of serum potassium. Contraindications related to hyperkalemia include a thermal injury greater than 24 hours old, (MacLennan N, 1998) although upregulation of receptors likely does not become clinically relevant until postburn day 5. Therefore, it is safe to use succinylcholine for RSI in most acute burns. It is contraindicated in patients with crush injury or rhabdomyolysis with hyperkalemia, (Gronert, 2001) congenital or acquired myopathies, conditions of subacute and chronic upper and motor neuron denervation including paralysis and polyneuropathy of critical illness, (Reynolds SF, 2005) a history of malignant hyperthermia and pseudocholinesterase deficiency. In addition, succinylcholine is reported to raise intragastric and intracranial pressure due to muscle fasciculations and may contribute to increased intraocular pressure. It should be used with caution in patients with injury to the brain and penetrating injury to the globe, although the evidence that succinylcholine raises intraocular pressure is anecdotal at best. (Vachon CA, 2003)

Nondepolarizing Agents

Nondepolarizing NMBAs, through competitive blockade of acetylcholine transmission at postjunctional, cholinergic nicotinic receptors, provide a paralytic alternative for those injured patients in whom succinylcholine is contraindicated. The aminosteriod compounds, including rocuronium, pancuronium, and vecuronium, represent the commonly used NMBAs for RSI and postintubation paralysis. Nondepolarizing agents for RSI are selected based upon the ability to best approximate the rapid onset and elimination of succinylcholine. The most intensively studied nondepolarizing agent utilized for RSI is rocuronium, which exhibits short onset and intermediate duration of action. In a recent Cochrane Database analysis comparing rocuronium to succinylcholine during RSI, rocuronium use was associated with inferior production of "excellent" intubating conditions, but equal "acceptable" conditions. (Perry J, 2003)Similarly, in a recent prospective, randomized comparative trial under emergent conditions, succinylcholine produced more rapid intubation and superior intubating conditions. (Sluga M, 2005) Despite the reported inferiority compared to succinylcholine, rocuronium has been shown to produce superior intubating conditions in comparison to vecuronium in the prehospital environment. (Bulger EM, 2002) When contraindications to succinylcholine exist, rocuronium produces acceptable intubating conditions and should remain in the RSI armamentarium as an alternative to succinylcholine.

REFERENCES

Bair AE, F. M. (2002). The failed intubation attempt in the emergency department: Analysis of prevalence, rescue techniques, and personnel. Journal of Emergency Medicine, 23(2), 131-140.
Bozeman WP, K. D. (2006). A comparison of rapid-sequence intubation and etomidate-only intubation in the prehospital air medical setting. Prehospital Emergecny Care, 10, 8.
Brown EM, K. D. (1979). A comparison of rapid-sequence intubation and etomidate-only intubation in the prehospital air medical setting. Canadian Anaesthia Society, 26, 489.
Bulger EM, C. M. (2002). An analysis of advanced prehospital airway management. Journal of Emergency Medicine , 23(2), 183-189.
Cohan P, W. C. (2005). Acute secondary adrenal insufficiency after traumatic brain injury: A prospective study. Critical Care Medicine, 33, 2358.
Davis DP, O. M. (2003). Paramedic administered neuromuscular blockade improves prehospital intubation success in severely head-injured patients. Journal of Trauma, 54, 444.
El-Orbany MI, W. Y. (2003). Does the choice of intravenous induction drug affect intubation conditions after a fast-onset neuromuscular blocker? Journal of Clinical Anesthesia, 15, 9.
Gronert, G. (2001). Cardiac arrest after succinylcholine: Mortality greater with rhabdomyolysis than receptor upregulation. Anesthesiology, 94, 523.
Jackson, W. (2005). Should we use etomidate as an induction agent for endotracheal intubation in patients with septic shock?: A critical appraisal. Chest, 127, 1031.
Kovacs G, L. J. (2004). Acute airway management in the emergency department by non-anesthesiologists. Canadian Journal of Anasthesia, 51, 174.
Lee BS, G.-H. M. (2001). Pediatric Airway Management. CPEM, 2, 91.
Lev R, R. P. (1994). Prophylactic lidocaine use preintubation: A review. 12(4), 499-506.
MacLennan N, H. D. (1998). Anesthesia for major thermal injury. Anesthesiology, 89, 749.
Malerba G, R.-G. F. (2005). Risk factors of relative adrenocortical deficiency in intensive care patients needing mechanical ventilation. Intensive Care Medicine, 31, 388.
Marvez E, W. S. (2003). Predicting adverse outcomes in a diagnosis-based protocol system for rapid sequence intubation. Americain Journal of Emergency Medicine, 21-23.
Naguib M, S. A. (2003). Optimal dose of succinylcholine revisited. Anesthesiology, 99, 1045.
Pearson, S. (2003). Comparison of intubation attempts and completion times before and after the initiation of a rapid sequence intubation protocol in an air medical transport program. Air Medical Journal, 22(6), 28-33.
Perry J, L. J. (2003). Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev 1:CD002788.
Reynolds SF, H. J. (2005). Airway management of the critically ill patient rapid-sequence intubation. Chest, 127(4), 1397-1412.
Robinson N, C. M. (2001). In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurologic outcome? A review of the literature. Emergency Medicine Journal, 18(6), 453-457.
Rodricks MB, D. C. (2000). Emergent airway management: Indications and methods in the face of confounding conditions. Critical Care Clinics, 16, 389.
Rotondo MF, M. M. (1993). Urgent paralysis and intubation of trauma patients: Is it safe? Journal of Trauma, 34, 242.
Schreiber JW, L. C.-B. (2005). Prevention of succiny-lcholine-induced fasciculation and myalgia: A meta-analysis of randomized trials. Anesthesiology, 103(4), 877-884.
Schuh, F. (1982). The neuromuscular blocking action of suxamethonium following intravenous and intramuscular administration. Int J Clin Pharmacol Ther Toxicol, 20, 399.
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Sivilotti ML, F. M. (2003). Does the sedative agent facilitate emergency rapid sequence intubation? Achedemic Emergency Medicine, 10, 612.
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Sonday CJ, A. J. (2005). Thiopental vs. etomidate for rapid sequence intubation in aeromedicine. Prehospital Disaster Medicine, 20, 324.
Tagaito Y, I. S. (1998). Upper airway reflexes during a combination of propofol and fentanyl anesthesia. 88(6), 1459-1466 .
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Zonies DH, R. M. (1998). The safety of urgent paralysis and intubation (UPI) in the trauma admitting area (TAA):A review of 570 consecutive patients. Journal of Trauma, 43, 431.

HEAD INJURIES & MTP

Injuries are the leading cause of death in persons younger than 45 years old with approximately one-third of these deaths a result of head trauma. Traumatic brain injury (TBI) results from either direct or indirect forces to the brain matter.  Annually, in the United States, there are approximately 1.7 million nonfatal TBIs, 275, 00 persons hospitalized as a result of a TBI, and 52,000 persons who die from TBI. (Faul M, 2010) The costs for treatment of both acute and chronic TBI are estimated to be $60 billion dollars in 2000. (Finkelstein E, 2006)

The primary injury occurs directly to the brain at the time of injury.  The secondary injury, which in most case is the injury  that results in the demise or permanent disability of the patient, begins hours after the initial injury.  Secondary injury the brain begins to swell, and place pressure on the fluids within the skull, resulting in increased intracranial pressure (ICP).  If we look back at our college neuroanatomy classes, and dust the cob webs from our text books we would find the “Monroe-Kellie Doctrine”.  Which if you do not recall basically states that you head is a rigid box, and within that box there is brain, blood & cerebral spinal fluid (CSF).  As one element increases, one or both of the remaining elements must decrease as the box (the skull) is rigid and will not expand.

As the brain swells it initially causes a decrease in CSF and then blood. When blood is decreased to the brain, oxygen and vital nutrients are also decreased, which leads to further injury.  This new injury leads to more brain edema, and the cycle continues until the process is reversed of the patient dies.

It is important to note that research has shown that hypotension and hypoxia doubles the rate of death in the head injury patient.  This makes complete sense.  If the brain is being starved of oxygen the simple intervention is to provide more!  Normally,  the body provides a higher pressure (reflected as the cerebral perfusion pressure or CPP) to over come the ICP.  The pressure gradient allows for blood to move freely into the brain.  When there are signs and symptoms of increased ICP, and the body is suffering from hypotension the body is unable to overcome the pressure within the skull causing a decrease in blood flow.

We can see this in the following equation:

CPP (Normal 80mmHg) = MAP(Normal 70-110mmHg)-ICP(Normal 7-14mmHg)

NOTE: Minimum CPP is 70mmHg & Minimum MAP is 60-65mmHg.

I offer the following scenario for the purposes of this article:

EMS go to the scene of a motor vehicle crash. They obtain a patient and quickly bring him to your trauma room.  You get the following verbal report:

This is John Doe. He is an approximately 40 year old male, who was riding his motor cycle down the highway and was struck by a SUV.  Both the vehicles had an estimated speed of 65mph.  Mr. Doe was ejected 20 feet striking the road.  Mr Doe was not wearing a helmet and witnesses stated that he was unconscious and not moving for approximately 5 minutes.  Vitals are: Pulse 112, agonal respirations of 7, blood pressure 70/38.  There is blood from the right ear and nose, 6 inch laceration to the left head and visible deformity to the right femur. Two large bore IV’s have been established. C-spine precaution and spinal restriction in place. Hare traction applied.  EBL 1000 to 1500mL and 800mL normal saline has been infused.

Lets  pause and think for a moment. Is this patient hypoxic? Yep! It is a fairly safe assumption.  The patient has lost 1.5 liters of blood and has poor ventilation's. (What type or types of hypoxia do you think he has?).  So we intubate, because as we all know hypoxia kills brain tissue.  So no the patient has an ETCO2 of 35 & a SpO2 of 100%.  Well there is one problem solved.  We now calculate the mean arterial pressure (MAP) and inject it into our CPP equation (we will assume that the patient has a normal, but high ICP).

CPP= 48 - 14

CPP=34 (OH CRAP!!!)

So now inevitably some one starts pouring in the saline or ringer’s, but is this the right treatment for the current dilemma?  Absolutely not!  It is here when we just go ahead and bust out the Massive Transfusion Protocol(PRBC,FFP, and Platelets).  Mr. Doe requires and increase in oxygen carrying capacity and he needs to be volume expanded, both of which are not accomplished by crystalloid.  To put is bluntly in Mr. Doe’s case if what you are administering does not address at least one component of the lethal triad it should not be given.

So you as the expert clinician gives 4 units of PRBC’s, 4 units of FFP, and 4 units of platelets (and you have pushed them in hard and fast!)

Now your blood pressure is 86/40 with a MAP of  62.

Again we play the numbers game.

CPP=62-14

CPP=48 (Still not at 70!)

So what do you do now?  If you said crystalloid walk yourself into the bathroom look in the mirror and slap yourself...hard! Repeat the blood transfusion! Do it again and again and again if you have to.

The avoidance of secondary injury is essential! A single episode of hypotension (systolic blood pressure of <90mmHg) has been shown to increase mortality in the adult population by 50%.

The role of the ER/Trauma clinician & prehospital provider is to not only stabilize the patient but it is prevent further injury. We must remember that simple interventions have profound effects.  The prehospital provider giving 100% oxygen to prevent hypoxia, or  the nurse keeping the patient warm in the trauma room to prevent the progression of the lethal triad, these simple interventions are imperative to decrease the morbidity and mortality of patients.

REFERENCES

1. Thurman DJ, Alverson C, Dunn KA, et al: Traumatic brain injury in the United States: A public health perspective. J Head Trauma Rehabil 14(6):602, 1999

2. Wax W, McKenzie EJ, Rice DP: Head injuries: Costs and consequences. J Head Trauma Rehabil 6:76, 1991.

3. Chestnut RM, Marshall LF, Klauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34:216, 1993.

4. Robinson N, Clancy M: In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J 18(6):453, 2001.

5. Albanese J: Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology 87(6):1328, 1997.

6. Modica PA: Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression. Can J Anaesth 39(3):236, 1992.

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15. Servadei F, Murray GD, Teasdale GM, et al: Traumatic subarachnoid hemorrhage: Demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries. Neurosurgery 50(2):261, 2002.

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22. Finkelstein E, C. P. (2006). The Incidence and Economic Burden of Injuries in the United States. New York, NY, USA: Oxford University Press.

SHOCK & TRAUMA’S LETHAL TRIAD

Shock is defined as “a pathophysiologic state in which the circulatory system is unable to perfuse tissues and meet oxygen demand adequately.” (Revell, 2003) Shock should never be described by a blood pressure.   A blood pressure is a poor indicator of the patients overall perfusion. 

Everyday, clinicians are faced with trauma’s lethal triad, which is comprised of hypothermia, acidosis and coagulopathy. (Rotondo M, 1997) When the clinician fails to address each aspect of the triad the results quite often result in fatal consequences.  The good news is that small interventions that address each arm of the lethal triad are both cost efficient and rather simple.

HYPOTHERMIA

We are all well aware of the alphabetic mnemonic is widely published in a number of trauma text books and manuals (For those of you who are not: A: Airway, B: Breathing, C: Circulation, D: Disability, E: Expose), unfortunately the “E” has turned out to be a double edged sword.  Prehospital providers have become samurai with their trauma shears and literally within mere minutes can have the victim of a trauma completely exposed to the elements and strapped to a hard plastic board.  The prehospital provider then expedites the patient the closest trauma center where the staff expose the patient again (assuming that the patient was that 1 in a billon who was covered with a Mylar blanket) and begin to infuse copious amounts of room temperature intervenous fluids.  At which point the patient is taken to CT (notoriously cold, even to the staff, and yes that is why the CT techs are always wearing sweaters), followed shortly there after by a trip to the operating room.  During this typical scenario, did anyone notice that the issue of hypothermia might have started to become problematic?

So why focus on something so simple?  Can a lowered body temperature really make that big of a difference?   YES!  Think of hypothermia as having its own triad.

Anticoagulation:

The clotting cascade, an item of vital importance when dealing with penetrating trauma is adversely affected by temperature, as the temperature of the trauma patient decreases the bodies ability to halt bleeding decreases proportionately, the body quickly looses is ability to clot. (Ferrara, 1990) (Watts, 1998)  Rohrer found that “enzymatic reactions of the coagulation cascade are strongly inhibited by hypothermia”. (Rohrer MJ, 1992)

In short, the clotting cascade has been shown to be adversely affected by temperature.  So to stop your patient from bleeding out keep them warm!

ATP Consumption:

            Adenosine triphosphate (ATP) is the human bodies fuel, without it the engine simply does not run.  When you look at the patient that has suffered a traumatic injury, there very quickly becomes an imbalance between supply and demand.  As catecholamines surge through he patient’s body, fuel (ATP) is used.  This causes a high demand, with no supply.  To further complicate the issue, like in the scenario detailed above the patient’s core body temperature begins to fall.  The patient then begins to shiver and shake generating his or her own source of heat.  This in turn increases the ATP expenditure, thereby stressing the already hypoperfused and hypoxic patient.

Patient Comfort:

            This is the portion of the article that generates the most laughter.  Patient comfort, how can we even consider patient comfort?  A patient presents to the trauma room after suffering multiple stab wounds.  Why must the clinician turn their attention from the fact that the patient is continuously bleeding from multiple stab wounds?   Well, firstly removing attention from active bleeding site is not the goal.  The goal here is to intervene on the lethal trauma triad before it spirals out of control. Addressing comfort is a simple intervention that both the nurse and physician can do, and this simple intervention can have monumental results.

           

It is well understood that being involved in a trauma can have far reaching physiologic as well as psychological effects.  The health care team can intercede before the patient is even admitted to the trauma room by altering the ambient temperature of the room.  Then once the patient arrives immediately following the primary survey warming blankets, and preferably a head covering should be provided for the patient. As discussed previously by maintaining normothermia the health care provider intercedes and decelerates the downward spiral of the clotting cascade.  This also prevents the patient from trembling, which utilizes already scarce and valuable ATP.  Lastly, the patient is in a particularly vulnerable state, to provide comfort, warmth, and a sense of safety and security serves to make a difficult experience a little psychologically more tolerable.

References

Watts, D. e. (1998). Hypothermic coagulopathy in trauma:effect of varying levels of hypothermia on enzyme speed, platlet function, and fibrinolytic activity. Journal of Trauma , 44 (5), 846-854.

Ferrara, A. e. (1990). Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfussion. Americian Journal of Surgery , 160 (5), 515-518.

Gubler K., G. L. (1994). The impact of hypothermia on dilutional coagulopathy. Journal of Trauma (36), 847-851.

Kashuk JL, M. E. (1982). Major abdominal vascular trauma: A unifid approach. Journal of Trauma (22), 672-679.

Revell, M. ,. (2003). Endpoints for fluid Resuscitation in hemorrhagic shock. The Journal of Trauma , 54, S63-S67.

Rohrer MJ, N. A. (1992). Effect of hypothermia on the coagulation cascade. Critical Care Medicine , 20 (10), 1402-1405.

Rotondo M, Z. M. (1997). The damage control sequence and underlying logic. Surg Clin North America (77), 761-777.

The Four Hypoxias

I have found that the easiest and best-understood method of addressing immediately life-threating conditions is to learn, understand and be able to intervene on the four types of hypoxia.

Hypoxia:

Hypoxia is a very general term that refers to a decrease in the amount of oxygen that is available to supply the cells and tissues of the body.  Hypoxia ultimately disrupts the intracellular oxidative process and impairs cellular function leading to cellular death.

Hypoxia differs from another term “Hypoxemia” which refers directly to the decrease in arterial oxygen tension, the PaO2.  Unfortunately, if the clinician narrows his/her focus on only the PaO2 it

There are four types of hypoxia that can be easily identified. The types of hypoxia can be easily remembered if one recognizes the effects that they have human body. Additionally, most causes of death can be directly attributed to one of these four types of hypoxia.

Stagnant Hypoxia:

Stagnant hypoxia which is probably most frequently seen in the intensive care unit can be described as a condition which results in a reduction in the total cardiac output, a decrease in blood flow to various tissues, a collection or pooling blood in particular areas of the body, or other restriction which slows, decreases the amount of, or halts blood flow. Stagnant hypoxia ultimately interferes with oxygenation by interfering with the bodies’ oxygen carriers, hemoglobin. The hemoglobin is unable to freely pass to one or more areas of the body. In these patients, you may or may not see an alteration in overall respiratory status. This is to say, that the patient may not present with tachypnea. An example of stagnant hypoxia would be if one would extend their finger and placement tourniquet on the proximal end of the finger occluding blood flow. The tissues in the distal end of the finger would then be suffering from stagnant hypoxia. The clinician may also cause stagnant hypoxia via intragenic means. One example of this could be if the patient is receiving continuous positive pressure ventilation and the clinician sets the ventilator with high pressures the subsequent increase in intrathoracic pressure may result in narrowing or occluding vasculature.

Possible Causes of Stagnant Hypoxia:

1. Pulmonary Embolism

2. Cardiac Failure

3. Cardiac Arrest

4. Stroke

5. Hyperventilation

6. Extreme  Temperature

7. Positive Pressure Ventilation

8. Compartment Syndrome

Specific Clinical Features:

•   PO2-Areterial 95mmHg; Venous 25mmHg

•   %O2 Saturation- Arterial 97%; Venous 45%

Hypemic Hypoxia

The post operative, intensive care or trauma clinician most frequently sees this type hypoxia. This is seen when there is a reduction in the oxygen carrying capacity of the blood. This is to say that there is a lack of hemoglobin, which exists in the body. When there is a decrease in blood there is a decrease in oxygen-carrying capacity and therefore the tissues and cells of the body ultimately suffer for this lack of oxygen. We are all well aware that when patient presents to the trauma room status post gunshot wounds to the tour so we can expect that even though the patient may have an oxygen saturation of 100%. We understand that the patient because of blood loss is ultimately in hypoxic state. What do we do? We replace this lost volume with packed red blood cells increasing the oxygen carrying capacity of the body and we transport the patient to the operating room where bleeding can be controlled surgically. A patient may also present to the emergency room after being involved in a home fire. The patient's carbon monoxide levels may be significantly increased. As we all well know, carbon monoxide has a high affinity to hemoglobin than does oxygen.  The space on hemoglobin used for the carrying of oxygen is occupied by carbon monoxide displacing oxygen to form carboxyhemoglobin.  In this case the patient has enough oxygen in the body but the amount of available hemoglobin is markedly less

In the previous scenarios I have stated that the patient may present with an oxygen saturation level of 100%. This begs the question does the nurse, respiratory therapist, or physician have to place oxygen on the patients? The simple answer here is yes! The patient is still hypoxic on a cellular level and therefore find providing the patient with more oxygen we increase free oxygen availability.

Possible Causes of Hypemic Hypoxia:

1. Anemia

2. Hemorrhage

3. Carbon Monoxide

4. Drugs (i.e. Nitrates)

5. Hemoglobin anomalies

Specific Clinical Features:

•   PaO2 - Arterial 95mmHg; Venous 40mmHg

•   Decrease in hemoglobin.

Hypoxic Hypoxia:

The easiest of the four hypoxias to remember!  Simply, it is hypoxia resulting from the lack of oxygen!  This can be caused by a decrease in space used for the exchange of oxygen or a decrease in the availability of oxygen.  Therefore if ambient air at sea level has a oxygen content of 21% and because of the partial pressure of the atmosphere at sea level an individual is able to utilize all (or 100%) of that 21% of oxygen, giving the individual a SpO2 of 98%.  Conversely if that same individual begins to climb Mount Everest when approximately 22,000 feet above sea level is reached, although there is still 21% oxygen in the ambient air (this is a great test question) the partial pressure has changed, now the individual has a SpO2 of 60%.

Another example could be the patient, who, because of pneumonia presents to the emergency department with a SpO2 of 72% on room air.  There is still an ambient oxygen level of 21%, however because of disease process the lung walls begin to thicken and now the area that is used for gas diffusion is less, resulting in hypoxia.

Possible Causes of Hypoxic Hypoxia:

1. Low PO2 in inspired air- high altitude.

2. Decreased pulmonary ventilation- airway obstruction, paralysis of respiratory muscle, narcotics

3. Defect in exchange of gases through the membrane.

4. A-V shunts, cyanotic heart diseases.

Specific Clinical Features:

•   PO2 - Arterial 40mmHg; Venous 2mmHg

•   %O2 Saturation - Arterial 75%; Venous 45%

Histotoxic Hypoxia

Last but not least, there is histoxic hypoxia.  In histoxic hypoxia there is no lack of available oxygen, and there is no pathologic condition that interferes with the diffusion of oxygen into the bloodstream.  In fact the issue is not getting oxygen to the hemoglobin, instead it is getting oxygen off the hemoglobin.

When a patient presents to the emergency room with signs and symptoms of hypoxia (increase in respiratory rate, drowsiness, disorientation, increase in heart rate or blood pressure, confusion or coma) status postindustrial fire, we immediately begin to assess the patient.   We note the following:

1.     RR: 50, HR: 119, BP: 168/100, SpO2 97%

2.     No carbon noted in the oral pharynx

3.     GCS 11, poor short term memory

4.     Hgb: 11.5,  carboxyhemaglobin:

5.     PaO2 95mmHg, PvO2 91 mmHg

6.     Skin: Peripheral & central cyanosis note.

7.     Intercostal, clavicular retractions with tracheal tugging.

8.     States “I can’t see its all blurry”.

9.     Chest X-Ray clear, with hyperinflation noted.

What lab test would you order? (Imagine you have the time to get any lab you want wait for the results and never compromise the patient’s health and safety).  Grab a cyanide level.  Cyanide acts by inhibiting the cytochrome oxidase enzyme system ultimately interfering with the body’s ability to use oxygen.

Possible causes of Histotoxic Hypoxia:

1. Cyanide Poisoning.  

2. Alcohol or drug ingestions.      

3. Metabolic disorders.     

4. Carbon monoxide can also be a hypemic as well as a histoxic hypoxia.

Specific Clinical Features:

•   PO2 - Arterial 95mmHg; Venous 90mmHg

•   %O2 Saturation - Arterial 97%; Venous 96%

Treatment of Hypoxia & Conclusion:

The treatment of any of the four types of hypoxia must be to provide oxygen, immediately followed by treatment of the underlying cause.  This may be intubation, administration of packed red blood cells, or an antidote for a particular toxin.  By having an understanding of the types of hypoxia and their underlying cause the clinician can better treat the patient in a rapid and efficient manner.