Biomedical subjects

John Ayling

Publications and source records attributed to John Ayling.

4 recordsLinked to original sources

PubMed2003

Ready to go.

The patient with a decreased level of consciousness in the absence of trauma presents difficult assessment and intervention problems. This is compounded when the history is vague or nonspecific. In this case, the patient's history of embolic CVA alerted providers to the possibility of another thrombus. This patient's sudden symptoms could have resulted from a clot in the brain, heart or aorta. This patient presented with an altered level of consciousness, vomiting and low blood pressure. As is typical in elderly female patients, she had an unusual presentation of an MI. A myocardial infaction is classified as either transmural or subendocardial. A transmural infarct extends through the full thickness of the myocardium and holds greater-risk of complications due to loss of functional muscle. In a subendocardial infarct, necrosis is limited to the endocardial surface. Although many elderly patients present with subendocardial MIs, this one had a large transmural MI. In general, the circumflex artery serves the lateral and posterior walls of the myocardium, and the right coronary artery (RCA) serves the inferior wall. In an anterior MI, the left anterior descending artery (LAD) is obstructed. This vessel serves the left ventricle, parts, of the septum and paillary muscles. The LAD is often referred to as the "widowmaker" because left ventricular infarcts have a high incidence of mortality. Occlusion of LAD can cause the usual damage of an MI, and can also cause fatal damage to the valves. This patient was in profound cardiogenic shock -- the left ventricle had infarcted and was unable to maintain cardiac output. Because of her recent stroke, she was not a candidate for thrombolytic medication. With ultrasonography, a large area of the anterior wall was found to be akinetic, or not functioning at all. In this care, the sourrounding myocardium not only has to pump blood with less muscle but also to "drag" the dead tissue. This results in a progressively higher rate of O2 cnsumption within the heart, further damage to the strained heart, and death. As cigarette smoking and obesity complete for the leading preventable cause of death in the United States, familiarity with cardiac anatomy and physiology 12-lead interpretation, pharmacology and electrical therapy is essential for all emergency providers

Aged↗

PubMed2003

Bugged.

This was a great save. The crew could easily have missed the presentation of anaphylaxis and let the window for treatment with epinephrine slip away. This patient was in anaphylactic shock. There were no signs that supported a traumatic injury, and that, combined with diaphoresis, urticaria and tachycardic central pulse, contributed to the suspicion of anaphylaxis. Anaphylaxis is classified as distributive shock. This type of shock is caused by profound systemic vasodilation, and the heart is unable to increase output enough to maintain blood pressure. Other causes of distributive shock include sepsis and spinal cord injury. It is rare to have both hypotension and wheezing in such cases. In an anaphylactic reaction, an allergen, such as a food protein, medication, insect venom or latex, is introduced into the body. The mast cells of the immune system have a protein on their surface called IgE antibodies (Immunoglobulin E). The mast cells are filled with histamines [table: see text] and leukotrienes, which are chemical mediators. These are released when the allergen reacts with the IgE antibodies. When these mediators are released, they cause smooth-muscle constriction in the respiratory and gastrointestinal tracts, resulting in wheezing, stridor, nausea, vomiting and diarrhea. They also cause vascular dilation, leading to edema and urticaria. Most patients will present with either profound vascular effect (shock) or wheezing; this is a rather rare presentation of a patient having both. The medication best suited to counteract the effects of these medicators is epinephrine. Epinephrine is an alpha- and beta-agonist, acting to constrict the vasculature and dilate the smooth muscles in the bronchial tree. Antihistamines can alleviate symptoms of anaphylaxis, but should only be used in addition to epinephrine, not as a substitute. In life-threatening reactions, epinephrine must be given quickly and in a form that the body can distribute. Use of the subcutaneous route with a solution mixed at 1:1,000 dilution is appropriate in most patients, but if the patient is in profound shock and not perfusing the skin (pale, cold, clammy skin), then a more diluted concentration must be given i.v. at a slow rate (1 cc every minute of the 1:1,000 dilution) until the patient recovers. If i.v. access is delayed or not available, give the 1:1,000 dilution intramuscularly, in the tongue or down the endotracheal tube. Refer to your local protocols for dosage, but the usual dose of epinephrine is 0.3-0.5 mg, or 0.01 mg/kg in a child. There are more than 40 million people in the U.S. with allergic histories that place them at risk for developing anaphylaxis. Each year over 5,000 deaths are attributed to anaphylaxis. The risk of death from anaphylaxis increases with a more rapid onset of signs and symptoms. Up to 25% of patients will experience a biphasic reaction. This means there is a recurrence of symptoms several hours after the initial reaction, and it is prudent to observe patients for a period of time following their initial treatment.

Adult↗

PubMed2003

Dialysis crisis.

Explore the source record for details and available documents.

Death, Sudden↗

PubMed2002

Managing head injuries.

The patient who presents with a serious head injury is often very difficult to manage. The airways is of primary concern; adequate ventilation must be provided and aspiration protected against. Recent studies suggest that hyperventilation may be as beneficial as was earlier believed. As the pCO2 level decreases, vasoconstriction occurs. If the level falls too low, cerebral perfusion is restricted, and profound cerebral anoxia may ensue. Current standards call for a ventilatory rate to allow for moderate respiratory alkalosis, in theory to mildly constrict teh vessels but still provide adequate perfusion. Arterial blood gas analysis in the ED is the definitive measurement of airway management in the field. Remember that the anatomy of the meningeal layers places the arteries primarily in the epidural space and the veins in the subdural space. A bleed in the epidural space often presents with a rapid onset of signs and symptoms, as was obvious in this traumatized patient. When a bleed occurs in the subdural space, the onset is usually more insidious, and an accurate history is a key to field diagnosis. As the hemorrhage expands, compression displaces the brain within the cranial vault. This displacement causes pressure to be exerted on the medulla of the brainstem. Cushing's Traid is a result of this pressure on the medulla and is evidence by the pulse slowing while systolic blood pressure rises and respirations become ataxic. Vomiting is often associated, and as the bleed continues, herniation syndrome begins. Decorticate posturing is displayed, followed by decerebrate posturing if relief is not provided. It is important to distinguish between decorticate and decerebrate posturing. It is important to distinguish between decorticate and decerebrate posturing. An easy way to remember the differences is to picture the anatomy of the brain. The cerebral cortex lies above the cerebellum, so when a patient's arms flexed up toward the face , he is pointing to his "core" (de-cor-ticate). As the arms extend downward, he is pointing to his cerebellum(de-cere-brate). T o manage the head-injured patient, it is imperative to anticipate potential developments, as well as protect against underlying injuries that may not be fully evaluated until arrival at the ED. Cervical spine often accompany head injuries, and full spinal immobilization is a mandatory precaution in all presentations. With the expanding hematoma found on this patient's neck, vascular damage ws obvious and contributed to the suspicion of spinal injury. As the intracranial pressure rise, vomiting and seizures are common. Placement of an endotracheal tube and having suction equipment ready are the best tools to prevent against aspiration. It is possible to angle the long spine board 10-15 degrees, exercising caution to ensure the patient's spinal alignment is not manipulated during the process. Seizures are usually treated with anticonvulsants like Valium. When a seizure accompanies a head injury, it is a direct result of the increased intracranial pressure and has a generally poor response to Valium, as the underlying cause of the seizure still exists. In this case, the patient had a full neuromuscular blockade, and any seizure would not have been recognized as long as the paralytics were on board. Early notification to the ED is essential, reporting all findings and interventions. This can alert them and give them the opportunity to prepare specialized equipment, such as CT scanners, mechanical ventilators, etc. Also, consider transportation options and the length of time to definitive care, including neurosurgical evaluation. This patient needs to be seen in a trauma center capable of the most thorough evaluation and management. Evacuation by air ambulance may be the most appropriate method of transport.

Craniocerebral Trauma↗