Anesthesia for the emergency patient (Proceedings)

As with any trauma patient presented to triage, a thorough pre-operative assessment must be performed and patient assessment begins with the first step inside the door. The traumatized patient will have altered physiological responses that will in turn alter the pharmacokinetics of the agents commonly used to provide anesthesia. Never labor under the assumption that your trauma patient was a previously healthy patient or even that the patient arrives with an empty stomach. Many patients are presented with under-lying pre-existing physical conditions.

Always presume your trauma patient to be in pain, respect and handle him accordingly during the assessment and surgical preparatory period.

Ideally, anesthesia should not be initiated until the vital organ function has been stabilized. Patients who have under gone severe trauma should be considered candidates for developing some type of shock. The ultimate result of any type of shock is the inadequate tissue perfusion thus leading to subsequent tissue oxygen debt. The goal of the triage team and nurse anesthetist should be, if at all possible, ensuring the airway is patent. Supplemental oxygen can be administered via tight fitting mask IF it does not cause excitation, or by flow by.

Ventilation should be assessed by observing the work of respiration and by the use of pulse oximetery to evaluate the oxygen saturation. It is frequent that multiple injuries to the respiratory system occur during thoracic trauma.

Optimizin the physiological function of the cardiovascular system includes normalizing the heart (pump) function and the maintaining the circulating volume in order to provide tissue perfusion and oxygen delivery to all vital organs. Administration of shock volume IV fluids should be with the goal of resuscitation of systolic blood pressure to a minimum of 90 mm/Hg. Once volume has been re-established, the use of a positive inotrope may be considered to maintain cardiac output during anesthetic administration if necessary.

Monitoring patient vital signs should begin during triage and continued well through the post operative recovery phase. Each patient will require continued evaluation based on its affected organ system or systems.

Cranial trauma is frequently caused by blows, intentional or otherwise, falls, and mishaps with vehicles. Unless there are obvious wounds to the head, cranial injury is not always immediately obvious. Any patient that has incurred a head trauma should be a suspect of increased intracranial pressure whether as a result of hemorrhage, cerebral edema or any space occupying lesion.

Any patient presented with known/observed trauma to the head or a history of circling, head tilt, seizures, head pressing, abnormal gait, disorientation, unequal pupil size or facial paralysis is considered at risk for increased intracranial pressure.

Cerebral blood flow must be insured to provide constant delivery of oxygen and glucose to the brain. It is imperative to maintain normal systemic blood pressure to protect cerebral perfusion pressure.

Ventilation must be carefully monitored to maintain PaCO2 levels within normal range at a minimum. It is common in patients with brain injuries, once intubated, to try to maintain PaCo2 levels at a slightly decreased value i.e. between 32-29 mmHg to avoid an increase in cerebral blood flow. Hypercapnea will cause cerebral vasodilation which leads to an increase in cerebral blood flow thus increasing intracranial pressure.

Additional factors to consider when dealing with a cranial trauma patient that may cause an increase in intracranial pressure:

     » Pain

     » Overly aggressive IV fluid therapy

     » Inappropriate positive pressure ventilation

     » Excitation or struggling on the part of the patient

     » Any pressure on the jugular veins whether from neck lead, jugular phlebotomy or jugular catheter placement

Ocular trauma commonly seen would include proptosed globes, corneal lacerations or foreign bodies. It is essential for any trauma patient that the cardiovascular system be stabilized prior to inducing general anesthesia. In addition, normal intra-ocular pressure must be preserved to avoid further damage to the affected eye.

The Oculocardiac reflex relates to a spontaneous drop in heart rate due to pressure/traction on the eye or surrounding structures that incorporate the trigeminal and vagus nerves. This decrease in heart rate is usually responsive to relieving the pressure applied or by the administration of an anticholinergic agent. Bracycephalic breeds as well as pediatric patients have a higher incidence of occurance due to an inherent higher vagal tone.

See the above stated additional factors to be considered when dealing with the ocular trauma patient as these factors may contribute to an increase in intraocular pressure as well.

Tracheal trauma, while not very common in small animals, can be caused by bite wounds, impaled objects, vehicular accidents, diagnostic procedures such as transtracheal wash, misguided jugular venipuncture attempts, over inflation of endotracheal tubes (especially in the feline patient), improper use of rigid stylets during endotracheal intubation. Crushing or non-penetrating wounds may be caused by blunt force trauma or choke collars. These patients can present in a state of collapse and cyanotic of there is sufficient obstruction of the airway. While a rapid prep is performed for a tracheostomy, oxygen may be livered by inserting a large bore catheter or needle directly into the lumen of the trachea distal to the obstruction. Injuries not causing life threatening obstructive compromise may be stabilized and supplemented with oxygen via a tight fitting mask or oxygen hood. If the patients overall assessment indicates that there is no current or pre-existing organ dysfunction and the patient is in an anxious state due to the work of breathing

Thoracic trauma, approximately one third of the patients with blunt forelimb or hind limb trauma additionally incur thoracic injury. Pulmonary lesions usually continue to worsen within 24-36 hours.

These may include:

     » Pulmonary contusions- hypoxia often results from severe contusions as a result of V/Q mismatch. Overzealous treatment of blood volume restoration may lead to pulmonary edema and a further decrease of lung function.

     » Emphysematous bulla- these lesions should be suspected and ventilation should be with low tidal volumes (inspiratory pressure <12 cm.of water) and a higher frequency to maintain minute volume.

     » Hemothorax- aspiration of the thoracic cavity can/should be performed to provide a more normal space for lung inflation. Hemothorax may result from rib fractures.

     » Pneumothorax- aspiration of the thoracic cavity again should be performed to allow for normalization of intrapleural pressure. Nitrous oxide should not be used with patients with known pneumothorax. Ventilation should be of lower tidal volume and a higher frequency.

     » Diaphragmatic hernia- vastly reduces the available space for proper lung inflation. If at all possible elevate the patient to at least a 30 degree incline to help relieve lung compression, while oxygenating.

     » Fractured ribs- caution must be taken to prevent additional injury to the lungs by patient manipulation. Intercostal blocks using bupivicaine will provide analgesia and aid in hypoventilation due to pain post-operatively.

Preoxygenation of any patient with known or suspected pulmonary lesions can be achieved with a tight fitting mask and should ideally be left on for five minutes prior to induction. Small dogs and cats in severe respiratory distress may decompensate even with minimal handling. The use of an oxygen cage or an induction chamber while gathering the necessary supplies to immediately capture the airway, will provide an oxygen rich environment.

Burn Injuries/smoke inhalation: The presence of soot in the nostrils, facial burning and dyspnea should hasten the responder's effort to initiate life saving measures. The immediate concern with these patients will be protection of the airway, venous access, fluid resuscitation and pain management. Capture of the airway should be achieved using agents including analgesic properties, a sterile endotracheal tube (low pressure high volume cuff) lubricated with sterile lidocaine gel. Propofol, thiopental, etomidate, benzodiazepines and inhalant agents do not provide any analgesia. Patients should be provided with 100% oxygen at the earliest possible moment. Pain management should include agents with pre-emptive properties i.e. lidocaine, ketamine with the addition of an opioid.

Burn patients are often presented with the additional trauma of smoke inhalation. Dermal burns seen in human medicine appear to have inflammatory cells sequester in the lungs thus causing more pulmonary edema than simple smoke inhalation. Regardless of the extent and severity of the burns, once the primary patient survey has been completed, analgesia should be provided. These patients should always be assessed while providing supplemental oxygen and the necessary equipment to capture the airway should the need arise. Hypovolemia in these patients is due to the fluid loss at the site of injury as well as vasoconstriction. Keep in mind that with the fluid loss, decreased protein contributes to not only decreased oncotic pressure but renders greater availability of the analgesic agents as the majority of the agents used are protein bound. It is ideal to start with ¼ to ½ dose of the agent and titrate to effect.

Blunt force abdominal trauma may involve several organs as in splenic/liver ruptures, kidney/ bladder rupture or avulsion or bowel perforation. This type of trauma combines crushing, stretching and shearing forces. Of prime importance with blunt force trauma patients is stabilization and the awareness that controversy still sounds taking a patient with a hemoabdomen credited to blunt force trauma to surgery too early. The exception to this would be the kidney that is avulsed from the aorta and causing life threatening hemorrhage. Should free air be noted on abdominal radiographs, this is considered an emergency exploratory laporotomy.

Penetrating wounds are more easily recognized but do not always reveal the damage to underlying body systems. Impaled objects should be stabilized until the patient has been fully evaluated and body systems supported until diagnostics have been performed.

Bite wounds can cause penetrating wounds as well crushing/tearing injuries. Bite wounds may actually penetrate a body cavity, thus allowing a portal for bacterial infection.

Premedication of trauma patients should take into consideration the analgesic agents previously administered during the triage/assessment period, the cardiovascular stability of the patient and the effect of the agent of all body systems. As previously mentioned, the trauma patient will require decreased dosages of analgesics due to altered physiological response on the part of the patient. Consider the procedure to be performed and the anticipated pain associated with the surgery when making your drug selection. Anesthesia should be designed to incorporate multiple agents, thus decreasing the adverse effects of any sole agent. Ideally, these agents should have the ability to be antagonized or reversed should the need arise

Anticholinergics may or may not be indicated and should not be "routine" as there is no "routine" with a traumatized individual. Anticholinergics will increase heart rate thus increasing cardiac work and oxygen consumption. If there is an underlying systolic dysfunction, an anticholinergic can decrease myocardial perfusion by decreasing diastolic filling time due to an increased heart rate. The goal with premedication should be to provide analgesia as well as decreasing the amount of induction agent required.

Agents increasing intracranial/intraocular pressure should be avoided in those patients with cranial and or ocular trauma such as ketamine.

The following listed multimodal combinations may be added to IV crystalloid fluids and delivered at either 10ml/kg/hr or 5ml/kg/hr using the following table adapted from Dr. W. Muir, Chapter 9, Small Animal Anesthesia and Analgesia, Dr. G. L. Carroll, editor, Blackwell publishing, 2008