True Medical Emergencies

It is not only traumatic injuries that can be suddenly lethal to prehospital patients. There are several medical conditions which, if left undetected, or misdiagnosed and untreated, can be rapidly fatal. These conditions can easily be confused for other, more benign problems. This article reviews a few of these lethal conditions and their sometimes discrete signs and symptoms to help you better manage your patients’ care and improve their chances of survival.

Pulmonary Embolus

A clot that forms in one part of the body and travels in the bloodstream to another part of the body is called an embolus. A pulmonary embolism is a sudden blockage in a lung artery, usually due to a blood clot that traveled to the lung from the deep veins of the leg. More than 600,000 people in the United States have a pulmonary embolism each year, and more than 60,000 of them die. Most of those who die do so within 30–60 minutes after onset of symptoms.1

The majority of patients with pulmonary emboli have an underlying clinical predisposition. Fewer than 10% of the patients have no discernible cause for deep venous thrombosis (DVT) at the time of presentation.2 Deep venous thrombosis, just like it sounds, is a condition where blood clots form in the deep veins of the lower legs. Conditions like immobilization, surgery, fracture, malignancy, thrombophlebitis, trauma, estrogen therapy, obesity, myocardial infarction and stroke all increase the likelihood of DVT. Surgical patients are commonly given venous support stockings for their legs and encouraged to move around after surgery to prevent these deep clots from forming and traveling to the lungs.

In pulmonary embolism, a piece of one of these clots breaks off and returns to the heart via the inferior vena cava, traveling through the cardiopulmonary circulation until it is too big to pass through a small vessel. Similar to a myocardial infarction and stroke, the clot prevents oxygenation of any tissues beyond itself. With this pulmonary embolus, lung tissue begins to die. If left long enough, this could develop into a pulmonary infarction; however, sometimes the emboli are so large that they can cause complete occlusion of a pulmonary artery and cause sudden death.

The clinical diagnosis of a pulmonary embolism is very difficult, therefore the prehospital provider’s level of suspicion must be high. The symptoms and signs of pulmonary embolus are nonspecific. Historically, a classical clinical triad was hemoptysis (coughing up blood), pleuritic chest pain (pain that increases with inhalation and decreases with exhalation) and difficulty breathing; however, this occurs in 20% or less of cases.2

The physical examination is equally unhelpful in diagnosing pulmonary embolus. The great majority of patients demonstrate an increased respiratory rate. The remainder of physical signs, which include an increased heart rate, elevated temperature, physical evidence of phlebitis, diaphoresis, edema, cardiac murmur, rales and cyanosis, are found in fewer than 50% of the patients who present with pulmonary embolus.2 Unexplained sudden onset of anxiety in a patient has been recognized as a common symptom of pulmonary embolus. In addition, for agencies that use pulse oximeters, a room air SpO2 of <80% in the patient with no other presenting or likely complaints places the patient in a high risk group for pulmonary embolus.3

Prehospital treatment is mainly oxygen therapy. ALS agencies may start an intravenous line, but there is no specific prehospital treatment regimen.

Emergency department and hospital diagnosis has been just as tricky. Chest x-rays of patients who are later confirmed to have had a pulmonary embolus are often abnormal, but in ways that are not specific enough to conclusively diagnose PE. Previously, the most reliable and sensitive tool has been pulmonary angiography—injection of dye into the pulmonary vessels—which is a complicated procedure with its own set of risks. Recent advances in computerized tomography (CT) scan technology have approached making spiral or helical CT scan the gold standard in diagnosing pulmonary embolus. In addition, a blood test known as d-dimer has been developed as a rapid screening test that measures a protein fragment left over after formation of a thrombus. This test has been used to triage patients into those who need advanced imaging and those who do not.

Aortic Emergencies

Much has been written on the subject of aortic emergencies, from the first well-documented case of aortic dissection when King George II of England died while straining on the commode to the first successful operative repairs by Dr. Michael DeBakey in 1955 and modern techniques of diagnosing and repairing thoracic aortic dissections. Conditions that affect the aorta can quickly turn into life-threatening emergencies that EMS providers need to be able to recognize.4 Aortic aneurysm, dissection and rupture are some of these conditions.

Aneurysm is defined as a dilatation of the aorta of greater than 150% of its normal diameter for a given segment. Dissection should not be termed dissecting aneurysm, because it can occur with or without aneurysmal enlargement of the aorta. In addition, thoracic aortic dissections should be distinguished from aneurysms and transections, which are caused most commonly by high-energy trauma (falls, high-speed MVAs). They are distinct entities.

Blood is pumped out of the left ventricle of the heart, through the aortic valve and into the aorta. The first part, the ascending aorta, arches, giving rise to the brachiocephalic, left common carotid and left subclavian arteries, then descends within the chest cavity. All of those parts make up the thoracic aorta. Once this large vessel penetrates the diaphragm, it is called the abdominal aorta. We will separate this discussion, starting first with the thoracic aorta, then covering the abdominal aorta.

Thoracic aortic aneurysm patients are most commonly white males, who are affected 2–4 times more frequently than women. Approximately 75% of dissections occur in those aged 40–70 years, with a peak in the range of 50–65 years. A genetic disorder known as Marfan’s syndrome is a potentially lethal connective-tissue disease characterized by skeletal, heart valve and ocular abnormalities. Individuals with this disease are at risk for aneurysmal degeneration, especially in the thoracic aorta.

The most common complaint of a patient presenting with a symptomatic thoracic aortic aneurysm, or dissecting aorta, is of tearing or stabbing pain in the chest or back. This is a vital description. Prehospital providers need to elicit this information from the patient and not just accept “my chest hurts.”

The location of pain may indicate the area of aortic involvement, but this is not always the case. Ascending aortic aneurysms tend to cause anterior chest pain, which may mimic a myocardial infarction. This is caused by the dissection interrupting flow to the coronary arteries and resulting in myocardial ischemia. Pain that is described in the neck or jaw indicates that the dissection involves the aortic arch and extends into the great vessels of the arch. Descending thoracic aneurysms are more likely to cause tearing or ripping back pain, localized between the scapulae. When the aneurysm is located at the level of the diaphragmatic hiatus, the pain occurs in the mid-back and epigastric region.4

This information is not included for EMS providers to diagnose the area of a suspected aneurysm, but more to make them aware that back pain or epigastric pain might be the only symptom of a life-threatening aneurysm and deserves a full evaluation. This description is not universal; some patients present with only mild pain that is often mistaken for musculoskeletal conditions located in the thorax, groin or back.

The pain of aortic dissection is distinguished from the intensity of the pain of acute myocardial infarction (AMI) by its abrupt onset. The truly sudden onset of chest pain is seen in few other conditions. Consider thoracic aortic involvement in the differential diagnosis of all patients presenting with chest pain that is especially acute, sudden and severe, and is maximal at its onset.4

In patients with symptoms suggestive of thoracic aortic emergency, blood pressure and pulse should be assessed for symmetry in both arms, and bilateral femoral pulses should be assessed. Discrepancy in blood pressure of greater than 20 mmHg between the arms is suggestive of aortic involvement. Hypotension is an ominous finding and may be the result of excessive vagal tone, cardiac tamponade or hypovolemia from rupture of the dissection. Neurologic deficits may be present, and syncope is also sometimes a presenting complaint.

Prehospital care should consist of ensuring adequate airway and breathing. Administer high-concentration oxygen, and assess for muffled heart sounds and jugular venous distension. ALS care involves starting two large-bore intravenous lines, as well as continuous EKG monitoring and assessment for evolving cardiac ischemia. Contact medical control for potential orders regarding blood pressure and heart rate management, as well as to authorize bypassing a nearby hospital in favor of a center with rapid surgical and intensive care capabilities.

Abdominal Aortic Aneurysm

The abdominal aortic aneurysm (AAA) is a relatively common, potentially life-threatening condition. It has a wide spectrum of presentations and should be considered in the differential diagnosis for a number of symptoms. Ruptured AAA is the 13th-leading cause of death in the U.S., causing an estimated 15,000 deaths per year. White males have the highest incidence of AAA, with more than three-fourths of patients with AAA older than 60 years.5

Expanding AAA causes sudden, severe and constant low back, flank, abdominal or groin pain. Syncope may be the chief complaint, and pain may be a less significant symptom to the patient. Patients with a ruptured AAA may present in frank shock, as evidenced by cyanosis, mottling, altered mental status, tachycardia and hypotension.

At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital.5

Presence of a pulsatile abdominal mass is found in less than half of cases. It is more commonly seen with a ruptured aneurysm. In an obese abdomen, an AAA is more difficult to palpate. Even in 25% of patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery. Providers need not be afraid of properly palpating the abdomen, because no evidence exists that aortic rupture can be precipitated by this maneuver.5

Misdiagnosis is fairly common, because the classic presentation of pain associated with hypotension, tachycardia and a pulsatile abdominal mass is present in fewer than 30%–50% of cases. The leading misdiagnosis is renal colic, as dissection of the renal artery may produce flank pain and hematuria.

Prehospital care includes initiation of airway and breathing support as necessary. Use of military antishock trousers (MAST) to reverse shock due to ruptured AAA may seem beneficial, but it may actually be detrimental. While their application theoretically offers temporary stabilization by compressing the leaking AAA and expanding hematoma, an undesirable reduction in cardiac output also occurs.5 Local protocol and medical direction should be followed. ALS care involves the initiation of two large-bore intravenous lines with isotonic fluid. Transport to a facility with rapid surgical ability is warranted.

Subarachnoid Hemorrhage

The skull is the bony protective covering of the brain. After the bone is removed, the brain is protected by three layers of tissue called meninges. The first layer, closest to the skull, is the dura mater, which is Latin for “hard mother.” Hence, bleeding between the skull and the dura mater is an epidural hematoma. Peeling away the dura mater, you find the arachnoid mater, named because it resembles a spider’s web spread out over the brain. Bleeding between the dura mater and this arachnoid mater is termed subdural hematoma. Below the arachnoid mater is the pia mater, the brain’s final layer of protection, which is actually in contact with brain tissue. Bleeding in the space between the arachnoid mater and the pia mater is termed subarachnoid hemorrhage (SAH).

SAH comprises half of spontaneous atraumatic intracranial hemorrhages. SAH is a devastating condition with high morbidity and mortality, and, in the United States, it is associated with an annual cost of $1.75 billion. The annual incidence of aneurysmal SAH in the United States is 6–16 cases per 100,000 population, with approximately 30,000 episodes occurring each year. An estimated 15% of patients die before reaching the hospital. Approximately 25% of patients die within 24 hours, with or without medical attention. The mortality rate at the end of one week approaches 40%. Half of all patients die in the first six months.6

Approximately 80% of SAH cases occur in people aged 40–65 years, with 15% occurring in people aged 20–40 years. Only 5% of SAHs occur in people younger than 20 years. The incidence of SAH is higher in women than men by a rate of 3:2. The risk of SAH is significantly higher in the third semester of pregnancy, and SAH from aneurysmal rupture is a leading cause of maternal morbidity, accounting for between 6%–25% of maternal deaths during pregnancy.7

When an aneurysm ruptures, blood is released under arterial pressure into the subarachnoid space and quickly spreads through the cerebrospinal fluid around the brain and spinal cord. Blood under such pressure may directly damage local brain tissue, and the resultant swelling and irritation lead to increased intracranial pressure.

The signs and symptoms of SAH range from subtle prodromal events, which often are misdiagnosed, to the classic presentation of catastrophic headache. The history and physical examination, especially the neurologic examination, are essential. Sentinel (or warning) leaks that produce minor blood leakage are reported to occur in 30%–50% of aneurysmal SAHs. Sentinel leaks produce sudden focal or generalized head pain that may be severe. Sentinel headaches precede aneurysm rupture by a few hours to a few months, with a reported mean of two weeks prior to discovery of the SAH. In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia, malaise or, less commonly, neck pain. These symptoms may be ignored by the care provider unless a high index of suspicion is maintained for SAH.

A patient complaining of “the worst headache of my life” should be presumed to be having an SAH until proven otherwise. These words are used as the textbook definition of SAH and bear great weight in establishing a diagnosis and treatment plan.

Symptoms of meningeal irritation (neck or back pain increasing with movement) are also very common, but can present long after the headache. Seizures during the acute phase of SAH occur in 10%–25% of patients. Blood pressure elevation is observed in about 50% of the patients; myocardial ischemia is present in about 20% of SAH cases. The regular expected findings of an intracranial event, one-sided weakness, trouble speaking and/or swallowing, and facial droop may also be seen.

Treatment, as always, centers around the ABCs. All patients should be monitored for their ability to maintain their own airway, as this ability can be suddenly lost as the hemorrhage progresses. BLS care is traditional, and again involves contacting medical control for authorization to bypass a local hospital for a facility that is prepared for urgent advanced radiological and neurosurgical procedures. It should be stressed for ALS providers that intravenous beta-blockers, which have a relatively short half-life, can be titrated easily, do not increase intracranial pressure (ICP) and are preferred over nitrates, which elevate ICP. Medical control should be fully advised of the patient’s status so appropriate measures can be taken. Patients with signs of increased ICP or herniation should be intubated and hyperventilated. Excessive hyperventilation is to be avoided, as it may increase vasospasm and cerebral ischemia.7

Ectopic Pregnancy

Ectopic pregnancy is any pregnancy in which the fertilized egg implants outside the intrauterine cavity. More than 95% of ectopic pregnancies occur in the fallopian tubes. No site besides the uterus is suited to accommodate placental attachment or a growing embryo. As the embryo outgrows its space in the small fallopian tubes, the chance for rupture of the tube and hemorrhage increases. Ectopic pregnancy occurs in 19.7 cases per 1,000 pregnancies in North America and is the leading cause of maternal mortality in the first trimester, accounting for 10%–15% of all maternal deaths. Ruptured ectopic pregnancy is a true emergency.

Several factors increase the risk of ectopic pregnancy, but share a common mechanism: interference with fallopian tube function. These include pelvic inflammatory disease (PID), which is most often associated with infection from chlamydia or gonorrhea. These can be silent infections that a woman does not know she has. These infections can scar the fallopian tubes and prevent easy passage of the egg into the uterus. A previous ectopic pregnancy is also a significant risk factor, as is endometriosis and a history of cigarette smoking.

Historically, the hallmark of ectopic pregnancy has been abdominal pain with vaginal bleeding, usually occurring six to eight weeks after the last normal menstrual period. It is noted, however, that only 40%–50% of patients with an ectopic pregnancy present with vaginal bleeding and 75% may have abdominal tenderness. Approximately 20% of patients with ectopic pregnancies are hemodynamically compromised at initial presentation, which is highly suggestive of rupture.8 It should be noted that many women have irregular menstrual cycles, so the six to eight weeks mentioned above must be taken in context and should not exclude a patient presenting with other symptoms. In addition, new contraceptive drugs are designed to only allow menstruation once every three months, so the history of the last menstrual period may be inaccurate.

It is noted in the literature that between 40%–50% of ectopic pregnancies are misdiagnosed during the initial visit to an emergency department.9 Identification of risk factors and a complete history and physical examination can raise your index of suspicion. For example, subtle changes in vital signs, such as mild tachycardia or lower-than- usual blood pressure, should prompt further investigation. This is especially true in the prehospital scenario when faced with a patient who wishes to refuse medical transportation because “a little abdominal pain is no big deal.” When in the field, without the benefit of lab results or ultrasound, your knowledge of potential problems could convince a patient to get the necessary medical attention to save her life.

BLS care should revolve around the ABCs, with repeated assessment of the patient’s hemodynamic status, including orthostatic changes in vital signs as indicated by local protocol. ALS care typically includes initiating two large-bore IVs with an isotonic solution (lactated Ringer’s or normal saline). Again, medical control may be needed to authorize transport to a facility prepared for immediate ultrasonography and gynecological surgery.

Conclusion

This article is designed to assist you in recognizing a few of the conditions which, if missed, may be rapidly fatal to your patient. These are all based on common chief complaints of our patients: shortness of breath, chest pain, abdominal pain and headache. Learning to ask the right questions, interpreting the answers and combining this subjective information with a complete physical exam should point you in the right direction to manage your patient. It should be noted that it is not necessarily the prehospital care that will make the difference for these patients, but the provider realizing that a lethal problem is occurring. You may wish to discuss your agency’s policies and protocols with your medical director and operational officers on managing the above conditions, including use of MAST, ALS protocols and which facilities in your area can handle these situations.

References

1. National Heart, Lung, and Blood Institute Diseases and Conditions Index. www.nhlbi.nih.gov/health/dci/Diseases/pe/pe_summary.html. Accessed on March 10, 2005.

2. Galvin J, Choi J. Clinical presentation on Pulmonary Embolus. www.vh.org/adult/provider/radiology/ElectricPE/Text/ClinPresent.html. Accessed on March 10, 2005.

3. Madigan Army Medical Center. Pulmonary Embolism. www.mamc.amedd.army.mil/clinical/standards/pe_alg.htm. Accessed on March 10, 2005.

4. Wiesenfarth J. Aortic Dissection. www.emedicine.com/emerg/topic28.htm. Accessed on March 10, 2005.

5. O’Connor R. Abdominal Aneurysm. www.emedicine.com/emerg/topic27.htm. Accessed on March 10, 2005.

6. Kazzi AA. Subarachnoid Hemorrhage. www.emedicine.com/emerg/topic559.htm. Accessed on March 10, 2005.

7. Newton T. Subarachnoid Hemorrhage. www.emedicine.com/med/topic2883.htm. Accessed on March 10, 2005.

8. Sepilian V. Ectopic Pregnancy. www.emedicine.com/med/topic3212.htm. Accessed on March 10, 2005.

9. Tenore JL. Ectopic Pregnancy. www.aafp.org/afp/20000215/1080.html. Accessed on March 10, 2005.