Anaphylactic Shock, A Life-Threatening Condition

Introduction

Anaphylactic shock is a life-threatening condition that can be fatal if treatment is delayed. Anaphylactic shock is defined as “an acute, life-threatening hypersensitivity reaction to a sensitizing substance” (Lewis, Bucher, Heitkemper, & Harding, 2017, p. 1590). When a patient is exposed to a sensitized allergen, the reaction escalates rapidly due to the release of inflammatory mediators ultimately causing vasodilation, circulatory failure, and respiratory distress (Lewis, Bucher, Heitkemper, & Harding, 2017). Due to the rapid progression of the condition, nursing students need to accurately identify clinical manifestations and provide immediate interventions. Otherwise, it can be a matter of life and death. Interestingly, anaphylactic shock is not being treated effectively according to a study in 2014. In a survey, out of 410 pediatrician participants with anaphylaxis scenarios, “just 11.3% of respondents answered all of the questions about management of mild anaphylaxis correctly, while 3.2% correctly answered all of the questions about management of severe anaphylaxis” (Kornusky & Ashley, 2017, p. 3).

According to CINAHL, “Anaphylactic shock is fatal in 0.65-2% of cases; 500-1,000 people die from the condition in the U.S. each year” (Kornusky & Ashley, 2017, p. 2). The purpose of this paper is to educate nursing students on the medical diagnosis of anaphylactic shock as an attempt to decrease the mortality rate of this condition. It encompasses the pathophysiology, signs, symptoms, assessments, diagnostic tests, complications, and interventions.

Pathophysiology

Anaphylactic shock is a severe reaction that is experienced by people when exposed to an allergen. Some of the most common allergens that can cause an anaphylactic reaction can be remembered by the mnemonic: MBLF (Many Boys Love Food) referring to medications, beestings, latex, and food. The antibody principally responsible for these reactions is immunoglobulin E (IgE) (Kemp, 2018). This paper will delve into the two categories that cause anaphylactic shock; immunologic and non-immunologic.

Immunologic

In immunologic anaphylactic shock, IgE is the main culprit. When exposed to the allergen in the lymphoid tissue, B cells start producing IgE cells with the help of T cells. These specially-formulated IgE cells only respond to the specific allergen it was created for. IgE cells then travel through the body’s circulatory system and tissues to attach to mast cells and basophils and continue to circulate throughout the body. Until the allergen is exposed near to the mast cell or basophil, the attached IgE interacts with the allergen. When multiple IgE antibodies are activated with the same allergen, it causes the cell to become activated thus initiating the inflammatory response by intracellular signaling by releasing mediators such as histamines and tryptase. The released cells either directly cause the inflammatory response to surrounding tissues or activate other inflammatory cells such as eosinophils. This process causes even more intracellular signaling and releases even more histamines and tryptase (Kemp, 2018). Histamines directly respond to surrounding tissue by causing vasodilation and encouraging the vessels to leak intracellular fluid from the vascular system. As a result, the blood pressure (BP) drops causing low oxygen perfusion to tissues and swelling. Consequently, shock is caused (Mannarino, 2014). In simpler terms, the allergen must have been sensitized in order for the reaction to develop. Therefore, the patient would have been exposed to the substance beforehand which may or may not have caused an allergic reaction at that time. During the first exposure, the immune system creates an antibody to detect and fight off the allergen to prepare for the next exposure.

Non-immunologic

In the less common non-immunologic anaphylactic shock, specific medications are the primary cause. These types of medications directly activate mast cells and basophils by the receptors without the involvement of IgE. This activation of mast cells and basophils act the same way as the immunologic anaphylactic shock with the production of inflammatory mediators such as histamine. Medications that can cause this type of anaphylactic shock include vancomycin and opiates (Kemp, 2018). It is important for health care providers to consider and observe any allergic reactions when providing such types of medications.

Clinical Manifestations

The two chemical mediators in response to IgE activation that cause clinical manifestations are histamine and tryptase. Low level of histamine can cause tachycardia. However, symptoms of hypotension, itching, bronchospasm, and headache are apparent when the levels are increased. Tryptase is a protease (enzyme that breaks down proteins) produced from mast cells specifically. It acts as a coagulant which facilitates hypotension and increases risk for clots. In rare cases, it can also cause disseminated intravascular coagulation (DIC) (Kemp, 2018).

Researchers from BioMed Research International, Tang et al. conducted a study in 2015 on inpatients’ clinical characteristics of anaphylactic shock. The study indicated that the most common clinical presentation of anaphylactic shock is on the skin (observed in up to 90% of studied cases). Integumentary presentations include hives, erythema, itching, and swelling (Tang et al., 2015). It happens due to the inflammatory response of histamine and other cell mediators released from IgE activation. Most common clinical manifestations shown in participants include, “Rash (62%), Dyspnea (46.3%), Loss of consciousness (38%), Nausea/ Vomiting (27.8%), Pallor (25%), excessive sweating (21.3%), palpitations (18.5%), abdominal pain (13%), facial swelling (12%), Rales heard in the lungs (10.2%), and dizziness (10.2%)” (Tang et al., 2015, p. 3). Hypotension is another expected symptom with anaphylactic shock due to histamine effects on the vascular permeability. Tang et al. (2015) studied the extent the BP drops during anaphylactic shock and found that, “the systolic pressure decreased from 117.4 ± 13.8 mmHg during baseline conditions to 54.3 ± 31.9 mmHg during episodes and the diastolic pressure decreased from 71.6 ± 13.6 mmHg during baseline conditions to 33.9 ± 21.4 mmHg during episodes” (p. 2). This study thus revealed how much the BP can drop during an episode of anaphylactic shock and some clinical presentations to assess while providing early treatment.

Assessments

If the patient is not active in anaphylactic shock, prevention is the key. A thorough health history is important to identify allergies and eliminate those allergens from the patient’s care. If a patient mentions an allergy, it is important to ask questions to explore the type of reactions they get from exposure, how they were exposed in the past, progression of condition, and if they have an EpiPen or use other treatments (Lewis, Bucher, Heitkemper, & Harding, 2017).

While in active anaphylactic shock, the primary assessment is airway, breathing, circulation (ABC’s) and management of life-threatening problems. Assessment should also include mental status to ensure adequate oxygenation to the brain tissue. Signs of angioedema should also be assessed with intubation equipment nearby in case of respiratory failure. Management of these will be discussed in the interventions. Secondary assessment is to determine patient’s history of allergies, allergen exposed to, how they were exposed, how long ago they were exposed, progression of symptoms, and interventions the patient has done (such as medications they took). Finally, it is imperative to assess vital signs and obtain remaining information concerning health history (Campbell & Kelso, 2018).

In general, it is important to assess patients for signs and symptoms of anaphylaxis. As mentioned earlier, one of the first manifestations shown is integumentary signs. Other signs that can indicate anaphylaxis are dyspnea, adventitious lung sounds, hives, pallor, swelling, tachycardia, and hypotension (Tang et al., 2015).

Diagnostic Tests

During the episode of anaphylactic shock, there is no test that specifically diagnoses the condition. It is purely based on the clinical presentation and history of exposure to allergens. However, laboratory tests, electrocardiogram (EKG), and chest x-rays are used to rule out other conditions and aide in the diagnosis of anaphylactic shock. Laboratory tests that simplify the anaphylactic shock diagnosis are a total tryptase serum and histamine in the plasma. Elevation in these levels indicates anaphylactic shock due to the mass production during the inflammatory process when exposed to a sensitized allergen. These tests are more accurate if there are baseline values to compare to after the anaphylactic shock episode. Total tryptase will have a maximum elevation above baseline values (up to 60 minutes) after onset of anaphylaxis and declines to baseline (approximately 2 hours after). Histamine will elevate 10 min after onset of anaphylaxis and declines to baseline by approximately 30 minutes. Therefore, blood should be drawn as soon as possible after the onset of symptoms to be the most accurate for histamine test and approximately 30-60 min after for the tryptase test (Schwartz, 2018).

Other tests should be considered to rule out additional conditions. Due to manifestations on the lungs and respiratory system, a chest x-ray should be done and evaluated to rule out other respiratory conditions, such as sepsis or pneumonia. It is also recommended to evaluate an EKG to assess for myocardial infarction (MI) (Schwartz, 2018). MI can develop due to the Kounis syndrome’s effect on coronary arteries – a complication of anaphylactic shock.

Complications

Complications that result from anaphylactic shock can be tragic. This section will explore some complications of anaphylactic shock to include cardiac and neurological conditions. One of the most tragic cardiac complications of anaphylaxis is sudden death. This occurs as a manifestation of the Kounis syndrome – an acute coronary syndrome that causes the coronary arteries to spasm due to mast cell activation and inflammatory mediators that are released in the inflammatory process during an anaphylactic shock episode. In addition to the pathophysiology of anaphylactic shock, coronary arteries are not being perfused adequately. Contributors of coronary deterioration include “systemic vasodilation, reduced venous return, leakage of plasma and volume loss due to increase vascular permeability, and diminished cardiac output” (Kounis, Soufras, & Hahalis, 2014, p. 228). The coronary arteries that are affected by Kounis syndrome, in addition to anaphylactic shock progression, can progress into a MI and ultimately sudden death (Kounis, Soufras, & Hahalis, 2014). Therefore, assessing an EKG for MI manifestations can lead to early detection and prompt treatment.

In 2018, Michelle Mangold and Mahboob Qureshi, physicians for Touro University Nevada College of Osteopathic Medicine, studied two aspects of anaphylactic shock complications; long-term effects and neurological manifestations. In this study, a patient had an extreme case of anaphylactic shock that resulted in loss of consciousness and four consecutive seizures induced by hypotension. The patient was later intubated and found with a Glasgow Coma Scale (GCS) score of 3. Fortunately, the patient recovered the following day with intact neurological function as evidenced by results from a computed tomography (CT) and magnetic resonance imagining (MRI). However, 8 months later, the patient indicated her vision changed by decrease in distance and depth perception and noticed halos while night driving. She also noticed short-term memory problems and a difference in hand writing. It is said that this may be due to long lasting effects as “the lasting sequela of visual and fine motor skill deficits may very well be a result of hypoxic injury to the brain… It is important to note that the patient had no pre-existing neurologic conditions nor symptoms of such” (Mangold & Qureshi, 2018, p. 4). This case is important to consider when treating patients with anaphylactic shock to make neurological assessments due to hypoxic effects on the brain. It is also significant to consider the increase of time in observation after anaphylactic shock treatment alongside more frequent follow-up appointments to check for long-lasting neurological effects.

Nursing Diagnoses

Nursing diagnoses that are relevant for anaphylactic shock indicate the priority of respiratory and cardiac problems including Ineffective Airway Clearance, Impaired Gas Exchange, and Decreased Cardiac Output (Ackley & Ladwig, 2014).

Ineffective Airway Clearance is relevant due to anaphylactic shock characteristics of bronchospasm, diminished lung sounds, dyspnea, and adventitious lung sounds. Goals should include airway patency. For example, the patient will always maintain a patent airway. This is accurate because if the patient is unable to have airway patency, intubation and other measures may be required. In addition to an accurate time frame, a patient should always have a patent airway even after discharge (Ackley & Ladwig, 2014, p. 129).

Impaired Gas Exchange is pertinent for anaphylactic shock due to the lack of tissue perfusion of oxygen caused by vascular permeability and vasodilation from histamine. Some manifestations are pallor, confusion, and tachycardia. Goals should include improvement of tissue perfusion. For example, the patient will have adequate oxygenation as evidenced by peripheral capillary saturation above 95% until discharge. In other cases, the patient will not show respiratory distress until discharge (Ackley & Ladwig, 2014, p. 375).

Decreased Cardiac Output is germane to anaphylactic shock because it describes the effects of histamine on the body with decreased tissue perfusion, edema, decreased central venous pressure, and dyspnea. Goals should include improvement of tissue perfusion as similar to improved gas exchange. For example, the patient will demonstrate adequate cardiac output as evidenced by blood pressure and heart rate within normal parameters until discharge (Ackley & Ladwig, 2014, p. 179).

Nursing Interventions

The nursing interventions for anaphylactic shock should be immediate once the onset of symptoms occurs. The first step is to remove the allergen causing the problem such as an intravenous (IV) medication. The cornerstone intervention for anaphylactic shock is the administration of an intramuscular injection of epinephrine as soon as possible. To prevent poking yourself with the EpiPen, remember the saying, “Blue to the sky, orange to the thigh.” Unless contraindicated, the patient should be placed in shock position by laying him/her supine with their feet passively elevated. Contraindications would be present if the patient is having respiratory complications of the upper airway (as they should be in high fowler’s position). If the patient is unable to keep a patent airway, as evidenced by stridor or respiratory arrest, intubation should be performed immediately upon assessment. If this is not the case, the patient should still be given supplemental oxygen with 15L/min via nonrebreather mask. The patient should then have two IV catheters inserted; one for emergency medications and the other for volume resuscitation with normal saline (NS) at a rate of 125 mL/hour. Epinephrine is usually infused slowly on the IV after the initial injected dose (Campbell & Kelso, 2018). The nurse should continue monitoring the patient’s vital signs including BP, heart rate, respiratory status, and peripheral capillary saturation. The patient should also be monitored for manifestations of fluid volume overload due to the large quantity of fluids that are being infused.

Epinephrine is an effective treatment for anaphylactic shock for its mechanism of action and preventing histamine and tryptase release from mast cells and basophils. It stops inflammation from progressing. Other beneficial mechanisms are vasoconstriction, bronchodilation, and decreased edema. Other pharmacological treatments that supplement epinephrine, but not used alone, are antihistamine and albuterol. Antihistamines are often administered to help relieve integumentary symptoms such as itching, redness, and hives (mostly caused by histamine). Albuterol is a bronchodilator that is administered to help relieve symptoms of dyspnea due to bronchospasm (caused by cell mediators) (Campbell & Kelso, 2018). Antihistamines and albuterol neither relieve symptoms of shock nor prevent the release of cell mediators from mast cells and basophils. For the same reason, it is paramount to administer epinephrine as priority and only use a supplement.

After treatment and observation period of anaphylactic shock, the nurse should provide comprehensive discharge education to prevent recurrence in the future. It is recommended for patients to schedule a follow up appointment with their immunologist for further evaluation of suspected allergens (Campbell & Kelso, 2018). In addition to an anaphylaxis emergency plan that outlines information about anaphylaxis and self-administering epinephrine, a prescription for an emergency EpiPen must also be given. Overall, it is important to educate the patient on how to avoid the allergen to prevent recurrence.

Conclusion

Anaphylactic shock is a life-threatening condition that can progress rapidly. Delay in epinephrine administration often results in death. To help combat the mortality rate of anaphylactic shock, this paper reviewed the diagnosis of the condition for nursing students. Therefore, nursing students could be more prepared for the rapid assessment and management for this life-threatening condition. To support this, this paper reviewed anaphylactic shock’s clinical manifestations, assessments, complications, and interventions.

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