Anaphylactic Case Study
Jim Palmer, a farmer aged 53 years had a hospital admission this morning with severe cellulitis on his left lower leg. Patient records indicate he had received one dose of Flucloxacillin 1gram IV as a slow bolus in the ED on reporting. He is giving a second dose of Flucloxacillin. Jim’s bell rings ten minutes later, and upon arrival, he is breathless and complains of a tight feeling in the throat, lightheadedness, and dizziness. As his assessment begins, his level of consciousness begins to reduce, progressively becoming drowsy and responding to voice only.
On examination:
- His RR is 26bpm.
- His systolic BP is 99mmHg on palpation
- He has a regular HR of 130bpm.
- A temperature of 37.4°C
- A SaO2 o 91% on RA
- His peripheries are cool and clammy
- His capillary refill time is >4secs
- There is wide spread urticarial rash and swelling of his lips, fingers, and toes.
- His blood glucose is 5.3mmols/ltr
Anaphylaxis
Anaphylaxis is a systemic IgE mediated hypersensitivity reaction (Kovacs, & Law, 2011). Anaphylaxis is severe, with a rapid onset of symptomatology. Acute phases may be mediated by antibodies as a result of exposure to antigens that promote the body’s production of Immunoglobulin E (Ig-E), or from a non-antibody mediated response, which results from substances causing the direct degranulation of mast cells and basophilic cells (Jarvis, 2016).
The pathophysiological mechanisms underlying anaphylaxis are as a result of the mast cell and basophil activation through the crosslinking of IgE and the aggregation of high-affinity receptors for IgE, FcRI (Craft & Gordon, 2016). Preformed mediators are then rapidly released from basophil/mast cells, including carboxypeptidase A, histamine, tryptase, and proteoglycans (Porth, & Porth, 2011). The downstream activation of phospholipase A2 (PLA2), closely followed by the activation of the lipoxygenase and cyclooxygenases produces metabolites of arachidonic acid, such as leukotrienes, prostaglandins, and the platelet activating factor (PAF) (Brown, 2007). The TNF-a (an inflammatory cytokine) is a preformed mediator released in the late phase of anaphylactic phase, acting in tandem with other chemokines and cytokines (Griffiths, 2008).
These mediators underlie the pathophysiological mechanisms of anaphylaxis. Histamine is responsible for the stimulation of vasodilation, with a concomitant increase in the permeability of the vascular, contraction of cardic muscles, HR and glandular secretion. Prostaglandin D2 causes bronchoconstriction, coronary and pulmonary vasoconstrictor and a peripheral vasodilator (Phipps, & Lugg, 2016; Tse & Rylance, 2009). Leukotrienes cause the constriction of bronchioles, increase the permeability of blood vessel, and promote the remodelling of airways. PAF increases vascular permeability in addition to being a potent bronchoconstriction. TNF-a is a potent activator of neutrophils, recruiting more other effector cells and enhances the synthesis of chemokines (Triggiani et al., 2008; Brown, 2007). According to Craft and Gordon, (2016), the synergistic and overlapping physiological effects of these cells and chemical mediators bring about the overall pathophysiological progression of anaphylactic reaction presenting as generalised angioedema and urticaria, cardiovascular manifestations including syncope, hypotension among others, respiratory symptoms including bronchospasms and other GIT effects such as cramping and nausea.
The Respiratory System
Inflammatory mediators released during anaphylaxis lead to pulmonary edema, swelling and vasoconstriction of bronchial tissues which cause breathing difficulties. The Respiratory narrowing will then present as chest tightness, chest pain, shortness of breath, coughing and wheezing. Other effects commonly found on examination include angioedema of the tongue, larynx and oropharynx, rhinitis, congestion and rhinorrhea. The overall picture produce by anaphylaxis is respiratory distress, which necessitates for emergency treatment. Untreated RDS causes respiratory arrest, a fatal condition (Phipps, & Lugg, 2016; Rosdahl, & Kowalski, 2008).
Obstruction of the airway is an emergency necessitating expert help. If untreated, airways obstruction leads to hypoxia, risking damage to the kidneys, brain and the heart whereas central cyanosis is a late diagnostic sign (Walls, & Murphy, 2008; Holbery, & Newcombie, 2016). In this case, Jim presents with breathlessness and complains of a tight feeling in the throat, all cardinal signs of an anaphylactic reaction. On examination, his RR is 26bpm. He also has a SaO2 of 91% on RA, which is below the normal range.
Managing the airway (A) involves establishment of a patent airway by either repositioning the head and neck of the patient or, doing an emergency cricothyroidotomy or endotracheal intubation (Simons et al., 2011). All these should be done while seeking expert help. Placing the patient in a supine position with elevation of the lower limbs is the recommended patient positioning. If Jim progresses into severe RDS, he may be put in a sitting position. Additional management will also include administration of oxygen at high concentrations using a mask with an oxygen reservoir. The flow should be sufficient (usually 15L/min) to minimise reservoir collapse during inspiration (Personage, 2010).
Oxygen at high concentrations should be administered to patients with airway obstruction using a mask with an oxygen reservoir. The flow should be sufficient (usually 15L/min) to minimize reservoir collapse during inspiration. A self-inflating bag should be used to give high concentration oxygen to patients with tracheal intubations (Walls & Murphy, 2008; Khan, & Kemp, 2011).
Breathing (B) should be accompanied by the immediate diagnosis of life threatening signs such as pulmonary edema (Brunner, & Smeltzer, 2010). Symptomatology associated with RDS, such as central cyanosis, sweating, abdominal breathing and use of accessory muscles should be sought (Simons et al., 2011). A high RR of >25bpm (normal being 12-20 bpm) is an illness marker, a warning sign of sudden patient deterioration. Physical examination will also include assessement of breath depth, breathing patterns (rhythm) and the symmetry in chest expansion, the presence of any chest deformities, and a raised JVP (Tse and Rylance, 2009). The percent concentration of oxygen inspired and SpO2 readings should be noted as hypercapnia cannot be detected by pulse oximetry (SpO2 may be normal if a patient is receiving supplemental oxygen in the presence of elevated PaCO2) (Jamieson, McCall, & Whyte, 2007; Rosdahl, & Kowalski, 2008). Respiratory treatment is dependent upon established pathological cause (Walls & Murphy, 2008).
The Cardiovascular System
During anaphylactic reactions, large quantities of histamine are produced. In human studies, injection of low doses of histamine into coronary vessels led to a rapid decrease in the mean aortic pressure with an increase in coronary blood flow mediated by activation of H1 receptors on vascular smooth muscles (Triggiani et al., 2008). Histamine also induces atrioventricular conduction blockades and arrhythmias in healthy individuals (Brown, 2007). Other effects include tachycardia and hypotension secondary to the release of catecholamines.
Eicosanoids including prostaglandins, leukotrienes and thromboxane have a role in cardiovascular manifestations of anaphylaxis (Craft, & Gordon, 2016). In the human heart, prostaglandin D2 (PGD2) and cysteinyl leukotriene (LTC4) is produced by mast cells. LTC4 and LTD4 induce a rapid and sustained increase in coronary vascular resistance, mainly due to their constrictive effect on intramural coronary vasculature. Similarly, the receptors CysLT1 and CysLT2 are expressed on cardio myocytes – their role in mediation of coronary vasoconstriction in still under study. The coronary effects pf PGD2 on humans is not known (Researchers postulate that eicosanoids play a role in the cardiac contractility, through the profound reduction of myocardial perfusion, overally leading to depression of cardiac cells and impairment of ventricular functioning – the primary hemodynamic events implicated in anaphylactic shock (Triggiani et al., 2008).
In the heart, PAF is released by mast cells, basophils, neutrophils, eosinophils and tissue macrophages. Animal studies have revealed the role of PAF in myocardial function. PAF is particularly associated with a profound reduction in coronary blood flow and major reduction in the contractile power of the heart. PAF’s interaction with cardiac ionic channels plays a role in its direct arrythmogenic activity (Triggiani et al., 2008). Additionally, PAF recruits and activates effector cells (eosinophils and neutrophils) in cardiac tissues. In atherosclerotic tissues, mast cell PAF contributes to plaque rapture which induces the aggregation of platelets and release of lytic enzymes. In systemic circulation, PAF induces peripheral vasodilation with relative hypovolemia and severe hypotension (Triggiani et al., 2008). Additionally, activation of platelets by PAF has been implicated in DIC in fatal anaphylaxis. The observations then suggest than PAF plays a major role in the reproduction of most, if not all, hemodynamic dysfunctions associated with severe anaphylaxis.
These cardiovascular events are relevant with Jims findings. On physical examination, Jims’ findings include an elevated HR (130bpm; normal range 60-100bpm), cool and clammy extremities and an increased capillary refill time (>4secs; normal <2s). His BP (99mmHg; normal range 90-140mmHg) and temperature (37.4°C; normal range 37-380C) are within the normal range.
Cardiovascular (C) management is dependent on the cause, are directed at controlling hemorrhages, replacing fluids and restoring perfusion (Kovacs, & Law, 2011). Exposure to the causative agent should be minimized or eliminated. One or more wide bored (14G or 16G) IV cannulas should be inserted as they enable the highest flow (Jarvis, 2016). Fluids to be infused should be isotonic solutions such as normal saline. A vasopressor, such as dopamine may be necessitated as the patient is to be transferred into an ICU.
The Skin and Integumentary System
Brunner and Smeltzer, (2010) note that the release of histamine in anaphylactic reactions increases capillary permeability, causing the leakage of plasma into extracellular tissues. Histamine causes blood vessel dilation, increasing capillary permeability which leads to escape of fluid into the extracellular spaces. The dilation and collapse of blood vessels additionally contributes to this edematous phenomenon. This results in edema manifesting as raised welts, or hives on the skin surface.
Because the H1 and H2 receptors are abundant in skin surfaces, exposure to the allergen causes their release, producing skin redness, itching and pain from the stimulation of sensory nerves (Triggiani et al., 2008). Management of dermatologic manifestation includes the patient avoiding scratching the skin, wearing lose clothes and avoiding wet, humid conditions. Administration of analgesics and prophylactic antibiotics may help deal with the pain and infections (Linton, & Watson, 2010; Younker, & Soar, 2010).
Blood Glucose and Assessment of Disability (D)
An elderly patient presenting with an anaphylactic shock should have their blood glucose measured to exclude hypoxaemia as it is a major cause of uncoinsuiusness (McCall & Whyte, 2007). Younker and Soar, (2010) elaborate that a rapid assessment of the patient’s conscious level should be done using the AVPU/GCS appropriately (Personage, 2010). Blood glucose should be measured using a rapid finger prick bedside testing method. Venous and arterial blood may be used in peri-arrest patients. Protocols for the management of hypoglycemia should be followed. Repeat blood glucose measurements to monitor treatment effects. In patients with diabetes mellitus national guidelines should be followed (Khan, & Kemp, 2011; Jamieson, McCall, & Whyte, 2007). Unconscious patients should be nursed in a lateral position if no airway protection measures are employed (Nolan, & Soar, 2012).
ISBAR Handover
Introduction: This is RN Amy from Ward 31 handing over Mr James Palmer, a 53-year old farmer who reported to the ED in the morning with severe cellulitis in his lower left leg.
Situation: Mr. Jim’s condition seemed under control until ten minutes later when his beside bell rang. Upon arrival, I found him flushed, breathless and complaining of a tight feeling in the throat and feeling lightheaded and dizzy. Jim has bilateral chest movements, and the depth of his breathing is shallow, I could hear an audible wheeze. He also has visible signs of central cyanosis. As I begun to assess the patient, I noticed his level of consciousness to be reducing, progressively becoming drowsy and responding to voice only.
Background: Mr. Palmer is a 53-year old farmer who reported to the ED in the morning with severe cellulitis in his lower left leg. On seeing the patient, he had already received one dose of Flucloxacillin 1-gram IV as a slow bolus in the ED. I administered his second dose of Flucloxacillin. On handover, the patient seemed to be deteriorating.
Assessment: The patient has an RR of 26bpm. On palpation, his systolic BP is 99mmHg. He has a regular HR of 130bpm, and a Temp of 37.4°C. His SaO2 is 91% on RA. The patient’s peripheries are cool and clammy. His capillary refill time is >4secs. There is wide spread urticarial rash and swelling of his lips, fingers and toes. His blood glucose is 5.3mmols/ltr.
Recommendation: the patient seems to be deteriorating. I recommend that the following
- The patient airway to be established.
- Attach a 12 lead ECG
- Laboratory investigations to include mast cell tryptase, UECs, and a Chest x-ray
- Adrenaline administration
- The patient to be put on high oxygen flow
- Administration of IV fluids
- Administration of chlorphenamine and hydrocortisone.
References
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