Saudi Journal of Kidney Diseases and Transplantation

CASE REPORT
Year
: 2021  |  Volume : 32  |  Issue : 6  |  Page : 1826--1829

Anaphylaxis: An Uncommon Cause of Rhabdomyolysis-Related Acute Kidney Injury


G. Shankar1, Debasish Mahapatra2, Vijoy Kumar Jha2,  
1 Department of Medicine, Military Hospital Wellington, Coonoor, Nilgiris, Tamil Nadu, India
2 Department of Nephrology, Medical Division, Command Hospital Air Force, Bengaluru, Karnataka, India

Correspondence Address:
Vijoy Kumar Jha
Department of Nephrology, Medical Divison, Command Hospital Air Force, Bengaluru - 560 007, Karnataka, India.
India

Abstract

Anaphylaxis is an acute, severe, and potentially lethal form of an allergic reaction. It can lead to a sepsis-like syndrome and multisystem involvement with complications. It can cause distributive shock with preferential blood supply to vital organs, at the expense of blood supply to skeletal muscle. Skeletal muscle ischemia leads to the fast depletion of myocyte energy source and a cascade of inflammatory reactions leading to myocyte injury and death. Myocyte lysis or rhabdomyolysis releases the cellular contents into circulation. Rhabdomyolysis is not an oft-discussed complication of anaphylaxis. We describe a 21-year-old male with no known comorbidity who presented with anaphylactic shock after consuming one tablet paracetamol + ibuprofen and was found to have rhabdomyolysis-related acute kidney injury.



How to cite this article:
Shankar G, Mahapatra D, Jha VK. Anaphylaxis: An Uncommon Cause of Rhabdomyolysis-Related Acute Kidney Injury.Saudi J Kidney Dis Transpl 2021;32:1826-1829


How to cite this URL:
Shankar G, Mahapatra D, Jha VK. Anaphylaxis: An Uncommon Cause of Rhabdomyolysis-Related Acute Kidney Injury. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Sep 30 ];32:1826-1829
Available from: https://www.sjkdt.org/text.asp?2021/32/6/1826/352449


Full Text



 Introduction



Anaphylaxis is considered an acute, potentially lethal syndrome resulting from the sudden release of mediators from mast cells, basophils, and macrophages. Toxin-related anaphylactic shock may lead to systemic reactions, including hemolysis, coagulopathy, rhabdomyolysis, and acute kidney injury (AKI).[1] Non-toxin-related anaphylaxis leading to rhabdomyolysis-related AKI is very uncommon. We report a case of a young male who presented as an anaphylactic shock with clinical features suggestive of impending respiratory arrest and subsequently developed rhabdomyolysis-related AKI requiring renal replacement therapy.

 Case Report



A 21-year-old male presented to the hospital with acute-onset swelling over the neck and submandibular area [Figure 1]. A clinical diagnosis of Ludwig’s angina was made. Contrast-enhanced computed tomography neck revealed diffuse soft-tissue swelling involving bilateral sublingual and submandibular spaces; diffuse swelling of bilateral aryepiglottic folds causing narrowing of airway [Figure 2]. Urgent tracheostomy was done as the patient developed stridor. Later, the case was seen by a physician. History revealed that the patient had taken one tablet of a nonsteroidal anti-inflammatory drug, paracetamol 325 mg + ibuprofen 400 mg, and experienced onset of symptoms within 30 min. A diagnosis of anaphylactic shock was made.{Figure 1}{Figure 2}

He was put on invasive ventilation, vasopressor support in view of refractory hypotension, steroids, and other supportive measures. The patient was noticed to have dark color urine and reduced urine output. Serum creatinine (SCr) increased from 1.1 to 2.5 mg/dL on the same day, with serum potassium (6.1 meq/L). He was transferred thereafter to a subspecialty center. At this hospital, SCr was 4.5 mg/dL, serum potassium - 6.5 meq/L, serum lactate dehydrogenase - 2391 IU/L, and creatine phosphokinase - 18,000 U/L. Urine dipstick was positive for blood.

He was started on an intravenous fluid-diuretic and alkalinization of urine regime. However, in view of progressive oligoanuria, rising SCr with hyperkalemia, and metabolic acidosis, he was initiated on hemodialysis (HD). He was weaned off invasive ventilation after three days, and tracheostomy was closed after one week. He received nine sessions of HD over 15 days, after which urine output improved and further HD were withheld. History was taken from the patient after recovery revealed no history of unaccustomed or severe exertion. He made a complete recovery and at follow-up after six months, he maintains normal renal function and muscle enzymes. The final diagnosis was anaphylaxis and AKI (rhabdomyolysis related). He was counseled against the use of ibuprofen for life.

The authors obtained all appropriate consent forms from the patient for the publication of this case report.



 Discussion



Anaphylaxis is often missed in patients with minor symptoms, which may even be missed by experienced physicians, making way for a more severe presentation after subsequent exposure to the same allergen. It is a severe form of an allergic reaction which is rapidly progressive and may even lead to death.[2] In humans, anaphylaxis is thought to cause a form of distributive shock leading to reduced venous tone and venous return. Besides, it causes fluid extravasation due to increased vascular permeability, leading to hypovolemia associated with depressed myocardial function.[3] It may affect any part of the respiratory tract, causing bronchospasm and mucous plugging in the smaller airways and laryngeal edema. In our case, the patient had presented with impending respiratory failure with stridor.

Anaphylactic shock may be complicated by anaerobic metabolism in skeletal muscles due to impaired oxygen consumption despite an increased partial pressure of oxygen. This impairment in cellular respiration has been attributed to an unregulated inflammatory process.[4] There may be more impaired skeletal muscle blood flow, possibly due to greater skeletal muscle vasoconstriction. There is a more rapid increase in interstitial lactate levels and a corresponding decrease in interstitial pyruvate levels, indicating the depletion of cellular energy stores.[5] This cellular energy store depletion and excessive agitation due to impending respiratory failure in anaphylaxis may be the possible factors leading to leakage of muscle cell contents, i.e., rhabdomyolysis as in this index case.

The myocytes are rich in electrolytes like potassium and calcium, muscle pigment-myoglobin, and sarcoplasmic proteins like creatine kinase, aldolase, lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase. Myocyte necrosis leads to the release of these contents into circulation, manifested by pigmenturia without hematuria. AKI is a common but not invariable manifestation of rhabdomyolysis.[4] In the present case, there was definitive evidence of rhabdomyolysis related to AKI in form of oligoanuria, myoglobinuria, raised muscle enzymes, azotemia, and hyperkalemia necessitating renal replacement therapy.

Anaphylaxis causing rhabdomyolysis is not so common. Perret et al have described a case of severe anaphylaxis due to succinylcholine, followed by rhabdomyolysis due to compartment syndrome in calf muscles, possibly aggravated by compartmental ischemia due to shock and local external compression in the lithotomy position.[6] Rhabdomyolysis can occur with the use of depolarizing neuromuscular blocking agents like succinylcholine, especially in individuals with genetic muscular diseases. Omar has described two cases of anaphylaxis and rhabdomyolysis; none of them were associated with AKI.[7] AKI caused by anaphylactic shock, triggered by a single dose of diclofenac sodium, has been reported in the literature.[8] However one dose of paracetamol + ibuprofen is unlikely to cause rhabdomyolysis.

In the case of toxin-related multisystem injury, optimal hydration is important to avoid kidney damage caused by rhabdomyolysis.[9] In toxin-related anaphylaxis like in multiple wasp stings, hemolysis and rhabdomyolysis are the two major factors that cause AKI due to severe toxic systemic reactions.[10] Rhabdomyolysis in our patients could be explained by refractory hypotension, agitation due to impending respiratory failure, anaerobic metabolism in skeletal muscles, use of sympathomimetic drugs, and steroid use.

Pathophysiology of kidney involvement in rhabdomyolysis includes tubular injury and obstruction. Tubular injury is caused by renal vasoconstriction and ischemia, which is contributed by the sequestration of a large amount of fluid in injured muscles and blood loss.[11],[12] Tubular obstruction is caused due to myoglobin-Tamm Horsfall protein cast, which is favored by acidic urine, volume depletion, and renal vasoconstriction.[12] Our patient was adequately managed with fluid resuscitation along with alkalinization of urine, resulting in excellent recovery.

There are no case reports of anaphylaxis causing rhabdomyolysis-related AKI in literature. This case report stresses the fact that AKI in the setting of anaphylactic shock may be due to multiple inciting factors leading to rhabdomyolysis.

Conflict of interest: None declared.

References

1Korman SH, Jabbour S, Harari MD. Multiple hornet (Vespa orientalis) stings with fatal outcome in a child. J Paediatr Child Health 1990;26:283-5.
2Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: Summary report − Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. J Allergy Clin Immunol 2006;117:391-7.
3Reber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol 2017;140:335-48.
4Fink MP. Bench-to-bedside review: Cytopathic hypoxia. Crit Care 2002;6:491-9.
5Dewachter P, Jouan-Hureaux V, Franck P, et al. Anaphylactic shock: A form of distributive shock without inhibition of oxygen consumption. Anesthesiology 2005;103:40-9.
6Perret D, Mahul P, Rochette Y, Auboyer C. Localized rhabdomyolysis after anaphylactic shock caused by suxamethonium. Ann Fr Anesth Reanim 1996;15:1193-5.
7Omar AS. Anaphylaxis and rhabdomyolysis. Any early relationship? Crit Care Shock 2012;15:88-94.
8Dhanvijay P, Misra AK, Varma SK. Diclofenac induced acute renal failure in a decompensated elderly patient. J Pharmacol Pharmacother 2013;4:155-7.
9George P, Pawar B, Calton N, Mathew P. Wasp sting: An unusual fatal outcome. Saudi J Kidney Dis Transpl 2008;19:969-72.
10Vachvanichsanong P, Dissaneewate P. Acute renal failure following wasp sting in children. Eur J Pediatr 2009;168:991-4.
11Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361:62-72.
12Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol 2000; 11:1553-61.