Acute Poisoning-Induced Rhabdomyolysis and Related Complications: A Report of Two Cases

Abstract

Rhabdomyolysis following acute poisoning is a rare complication. Acute poisoning with profenofos, an organophosphorus insecticide that irreversibly inhibits acetylcholinesterase, and Super Vasmol 33, a hair dye containing para-phenylenediamine, is associated with significant morbidity and mortality. Although rhabdomyolysis is an uncommon complication, it may precipitate acute kidney injury (AKI) and multiorgan dysfunction syndrome (MODS). Here, we report two cases of rhabdomyolysis following acute poisoning. The first case involved a 40-year-old nonalcoholic male admitted after self-ingestion of Profestar 50% E.C. (profenofos 50%). He developed rhabdomyolysis followed by AKI and MODS, requiring multiple hemodialysis sessions and other critical care support. His hospital stay was complicated by a hospital-acquired infection, which improved with antibiotic therapy. The second case involved a 15-year-old female with Super Vasmol 33 poisoning who developed neck edema and stridor, which improved after administration of epinephrine and hydrocortisone. Subsequently, she developed rhabdomyolysis and MODS, requiring dialysis. Both patients fully recovered and were discharged. Despite severe poisoning, both patients had favorable outcomes due to early recognition of rhabdomyolysis, prompt aggressive fluid resuscitation, timely renal replacement therapy, intensive care support, early airway management in the Super Vasmol poisoning case, and close monitoring with correction of metabolic and electrolyte abnormalities, resulting in complete recovery.

Introduction

Poisoning is a major public health concern, particularly in the developing world, contributing to substantial morbidity and mortality each year. According to WHO, unintentional poisoning caused approximately 84,278 deaths worldwide in 2019, resulting in the loss of five million disability-adjusted life years [1]. The mortality rate from unintentional poisoning has declined over the past decades. In 2000, the global mortality rate was estimated at 1.1 deaths per 100,000 population, which decreased to 0.8 deaths per 100,000 population by 2016 [2].

Organophosphate (OP) poisoning is a significant global health concern, particularly in agricultural regions. It mainly leads to three clinical syndromes: acute cholinergic syndrome, intermediate syndrome, and OP-induced delayed polyneuropathy. In addition, OP poisoning can rarely cause acute respiratory distress syndrome, rhabdomyolysis, acute kidney injury (AKI), subarachnoid hemorrhage [3], and multiorgan dysfunction syndrome (MODS).

The ancient science of cosmetology is believed to have originated in India and Egypt [4]. The earliest records of the art of dyeing hair with henna, indigo, and vegetable dyes date back to circa 2500 and 1550 B.C. in the Indus Valley civilization, where the preferred hair colors were black or orange-red [5]. Nowadays, the most commonly used hair dye is Super Vasmol. Super Vasmol is an emulsion-based hair dye widely used in India, and poisoning due to its ingestion is emerging as a major cause of suicide in the developing world because it is inexpensive and freely available over the counter [6].

Here, we report two cases of rhabdomyolysis and its related complications, one following OP poisoning and the other following Super Vasmol poisoning.

Case presentation

Case 1

A 40-year-old male was brought to the ED four hours after self-ingestion of Profestar 50% E.C. (profenofos 50%, an OP compound). On examination, his Glasgow Coma Scale score was 13/15 [7], pulse rate (PR) was 58 beats/min, blood pressure (BP) was 110/70 mmHg, and temperature was 98.6°F. The pupils were equally miotic and reactive to light. Fine crepitations were heard bilaterally in the lung fields, consistent with OP poisoning.

Emergency laboratory investigations showed a total leukocyte count (TLC) of 11,289/µL (neutrophils 91%, lymphocytes 7%), hemoglobin (Hb) of 13.0 g/dL, platelet (PLT) count of 151 × 10⁹/L, serum urea of 40 mg/dL, serum creatinine of 1.0 mg/dL, serum sodium (Na⁺) of 140 mEq/L, serum potassium (K⁺) of 3.5 mEq/L, and serum cholinesterase of 2,600 U/L (reference: 4,000-10,000 U/L). Viral screening, including HIV, hepatitis B surface antigen (HBsAg), and hepatitis C virus (HCV), was negative. ECG was within normal limits. Treatment was initiated according to WHO protocol with IV atropine and a pralidoxime infusion at 8 mg/kg/h after a loading dose of 30 mg/kg [8].

On Day 4, the patient’s vital signs were stable, and chest auscultation was clear, but he developed oliguria (urine output, 300 mL/24 h). Investigations revealed a TLC of 11,000/µL, Hb of 13.2 g/dL, PLT count of 162 × 10⁹/L, serum urea of 100 mg/dL, serum creatinine of 6.8 mg/dL, serum Na⁺ of 138 mEq/L, and serum K⁺ of 3.4 mEq/L. The patient was transferred to the medical intensive care unit (MICU), and hemodialysis was planned. Despite one hemodialysis session on Day 4, the patient developed anuria (urine output <50 mL/24 h). Investigations showed serum urea of 160 mg/dL, serum creatinine of 11.4 mg/dL, serum Na⁺ of 133 mEq/L, and serum K⁺ of 4.6 mEq/L. Ultrasonography revealed acute medical renal disease with increased cortical echogenicity and intact corticomedullary differentiation, as well as a bulky pancreatic parenchyma with minimal peripancreatic collection suggestive of acute pancreatitis (Figure 1).

Figure 1. Case 1: Ultrasonography of the abdomen showing bilateral acute medical renal disease.

Increased renal cortical echogenicity (black arrow) and prominence of the renal pyramids (red arrow).

Further investigations showed a urinary myoglobin level of 9,192.00 µg/L (reference: 0-1,000 µg/L), serum creatine phosphokinase (CPK) of 27,000 U/L (reference: 25-200 U/L), total bilirubin of 11.2 mg/dL (reference: 0.3-1.3 mg/dL), direct bilirubin of 9.8 mg/dL (reference: 0.1-0.4 mg/dL), serum glutamic-oxaloacetic transaminase (SGOT) of 1,200 IU/L (reference: 12-40 IU/L), serum glutamic-pyruvic transaminase (SGPT) of 2,300 IU/L (reference: 8-40 IU/L), alkaline phosphatase (ALP) of 321 IU/L (reference: <360 IU/L), serum lactate dehydrogenase (LDH) of 4,617 U/L (reference: 313-618 U/L), serum cholinesterase of 6,528 U/L, serum amylase of 226 U/L (reference: 25-86 U/L), serum lipase of 577 U/L (reference: <60 U/L), ionized calcium of 1.1 mmol/L (reference: 1.1-1.4 mmol/L), prothrombin time of 18.5 seconds, activated partial thromboplastin time of 35.6 seconds, and an international normalized ratio of 1.55. Viral markers, including hepatitis A virus (HAV) IgM and hepatitis E virus (HEV) IgM, were negative.

The patient was diagnosed with OP poisoning complicated by rhabdomyolysis and fulfilled the criteria for MODS, including AKI (Kidney Disease: Improving Global Outcomes (KDIGO) Stage III) [9] requiring renal replacement therapy, acute liver injury (ALI), and acute pancreatitis. He was treated with IV fluids, antibiotics, hemodialysis, and other supportive measures. Regular hemodialysis was performed through Day 10; however, despite six sessions, the patient remained anuric (<50 mL/24 h).

On Day 12, the patient developed a fever, and investigations were performed for an ICU-related infection. TLC was 19,130/µL (neutrophils 93.7%), and serum procalcitonin was 8.14 ng/mL (reference: <0.05 ng/mL). Screening for tropical infections, including malaria parasite (immunochromatographic test, ICT), dengue NS1 antigen and IgM antibody, Leptospira IgM, and scrub typhus IgM, was negative. Urinalysis and urine microscopy showed 10-20 pus cells/high-power field and granular casts. Broad-spectrum antibiotics were started at doses adjusted according to creatinine clearance after blood cultures were obtained.

By Day 15, urine culture showed no growth, and blood cultures showed no growth after 24 hours and 5 days of incubation using a fully automated BACTEC fluorescent technology system. The fever subsequently resolved. By Day 23, the patient remained anuric despite 19 hemodialysis sessions. On Day 24, urine output increased to 200 mL/24 h, and hepatic and renal function improved. From Day 24 to Day 40, a total of 14 additional hemodialysis sessions were performed. On Day 40, urine output increased to 800 mL/24 h, and renal and hepatic function further improved, allowing transfer to the ward. The day-wise biochemical and hematological investigations are shown in Table 1.

Table 1. Case 1: Day-wise hematological and biochemical investigations.

ALP, alkaline phosphatase; Hb, hemoglobin; PLT, platelet; SGOT, serum glutamic-oxaloacetic transaminase; SGPT, serum glutamic-pyruvic transaminase; TLC, total leukocyte count

Parameter	Day 6	Day 8	Day 10	Day 12	Day 15	Day 17	Day 20	Day 23	Day 26	Day 29	Day 35	Day 39	Day 41	Day 45	Reference range
TLC (/µL)	13,890	11,280	12,680	19,130	11,440	13,520	15,940	14,960	14,000	12,340	10,000	9,450	8,210	7,390	4,000-11,000
Neutrophils (%)	92.3	92.5	95.1	93.7	86.4	85.2	96.5	86	82.4	81.2	80	78.2	74.4	72.6	40-60
Lymphocytes (%)	2.9	2.8	2.6	2.5	6.8	7.4	1.2	8	9.2	10.1	12.5	18.4	19.5	22.6	20-40
Hb (g/dL)	13	12.2	10.6	10.1	8.3	7.8	8	8	8.5	8.5	9.2	9.6	10.1	10.2	11.0-17.0
PLT count (×10⁹/L)	91	133	220	267	322	419	413	335	412	234	212	176	154	151	150-450
Serum urea (mg/dL)	160	128	129	181	129	170	196	123	163	187	157	101	96	62	15-40
Serum creatinine (mg/dL)	14	10.9	12.7	18.7	16.8	18.1	19.5	19.4	16.5	14.7	12.3	9.6	6.1	3.7	0.5-1.2
Serum Na⁺ (mEq/L)	136	137	139	139	141	140	144	135	143	137	139	141	142	142	135-145
Serum K⁺ (mEq/L)	3.4	4.2	4.3	4.6	4.5	5.2	4.8	5.1	4.8	4.9	5.1	5	4.8	4.6	3.5-5.5
Total bilirubin (mg/dL)	10.1	12	15.1	4.5	4.1	3.4	NA	2.7	NA	2.8	NA	2.6	NA	2	0.3-1.3
Direct bilirubin (mg/dL)	9	8	12.1	3.4	2.8	2.4	NA	2.1	NA	1.6	NA	1.5	NA	1.2	0.1-0.4
SGOT (IU/L)	1,267	1,570	1,180	93	87	54	NA	67	NA	40	NA	44	NA	40	12-40
SGPT (IU/L)	2,334	1,837	1,326	114	100	24	NA	37	NA	30	NA	29	NA	28	8-40
ALP (IU/L)	331	745	789	967	716	736	NA	796	NA	681	NA	584	NA	412	<360

As urinary output and renal and hepatic function were fully restored, the patient was discharged on Day 46 after completing 33 sessions of hemodialysis. The day-wise trends in hematological, renal, and hepatic parameters are shown in Figure 2, and the overall clinical timeline is summarized in Table 2.

Table 2. Case 1: Clinical timeline.

AKI, acute kidney injury; ALI, acute liver injury; CPK, creatine phosphokinase; GCS, Glasgow Coma Scale; KDIGO, Kidney Disease: Improving Global Outcomes; MICU, medical intensive care unit; MODS, multiorgan dysfunction syndrome; OP, organophosphate; PR, pulse rate; TLC, total leukocyte count

Day	Clinical events	Key findings and interventions
0	Presentation with acute OP poisoning	Self-ingestion of Profestar 50% E.C. (profenofos 50%). Presented four hours after ingestion with a GCS score of 13/15, PR of 58 beats/min, miosis, and bilateral crepitations. Serum cholinesterase was 2,600 U/L. Gastric lavage, IV atropine, pralidoxime infusion, and supportive care were initiated.
4	AKI developed	Oliguria (300 mL/24 h). Serum urea was 100 mg/dL, and serum creatinine was 6.8 mg/dL. The patient was transferred to the MICU, and the first hemodialysis session was performed.
5	Rhabdomyolysis with MODS diagnosed	Persistent anuria (<50 mL/24 h) and serum creatinine of 11.4 mg/dL. Serum CPK was 27,000 U/L, and urinary myoglobin was 9,192 µg/L. ALI, acute pancreatitis, and AKI (KDIGO Stage III) were confirmed. Ultrasonography showed bilateral acute medical renal disease.
5-10	Intensive management	Serial hemodialysis, IV fluids, antibiotics, electrolyte correction, and supportive care. Persistent anuria despite six hemodialysis sessions.
12	Suspected ICU-related infection	Fever developed. TLC was 19,130/µL, and procalcitonin was 8.14 ng/mL. Blood and urine cultures were obtained. Broad-spectrum antibiotics were initiated. Tropical fever workup was negative.
15	Infection controlled	Blood and urine cultures showed no growth. The fever subsided with antibiotic therapy.
23	Persistent renal failure	Continued anuria despite 19 hemodialysis sessions.
24	Recovery phase	Urine output increased to 200 mL/24 h. Renal and liver function tests began to improve.
24-40	Progressive recovery	An additional 14 hemodialysis sessions were performed. Gradual improvement in urine output and biochemical parameters was observed.
40	Clinical improvement	Urine output increased to 800 mL/24 h. Renal and hepatic function markedly improved. The patient was transferred from the MICU to the general ward.
46	Discharge	Complete clinical recovery with restoration of urine output and improving renal and hepatic function. The patient was discharged after 33 hemodialysis sessions.

Figure 2. Case 1: Day-wise trends in hematological, renal, and hepatic parameters.

(A) TLC progressively normalized during hospitalization. (B) Serum urea and serum creatinine initially worsened because of AKI, followed by gradual recovery after repeated hemodialysis. (C) Liver enzymes (SGPT, SGOT, and ALP) progressively normalized, indicating recovery from acute hepatic injury.

AKI, acute kidney injury; ALP, alkaline phosphatase; SGOT, serum glutamic-oxaloacetic transaminase; SGPT, serum glutamic-pyruvic transaminase; TLC, total leukocyte count

Case 2

A 15-year-old female was brought to the ED two hours after self-ingestion of Super Vasmol 33 hair dye. On presentation, she had neck edema and stridor. On examination, PR was 100 beats/min, BP was 102/60 mmHg, respiratory rate was 30 breaths/min, peripheral oxygen saturation (SpO₂) was 82% on room air, and fine crepitations were heard bilaterally over the infrascapular areas. The pupils were normal in size and reactive to light.

In view of desaturation and stridor, the patient was transferred to the ICU. IV chlorpheniramine maleate, IV hydrocortisone, and intramuscular epinephrine were administered, along with other supportive measures and antioxidants. The patient was intubated and placed on mechanical ventilation. After one day, the edema subsided, and respiratory distress improved.

Investigations showed a TLC of 10,004/µL (neutrophils 80%, lymphocytes 11%), PLT count of 114 × 10⁹/L, Hb of 13.0 g/dL, serum urea of 40 mg/dL, serum creatinine of 1.1 mg/dL, serum sodium (Na⁺) of 138 mEq/L, and serum potassium (K⁺) of 4.3 mEq/L. Arterial blood gas analysis revealed compensated respiratory alkalosis. ECG was normal, troponin I was negative, and viral screening, including HIV, HBsAg, and HCV, was negative.

On Day 2, the patient developed oliguria with dark-colored urine (Figure 3). Investigations revealed serum urea of 100 mg/dL and serum creatinine of 4.6 mg/dL. Ultrasonography showed features of acute medical renal disease with increased cortical echogenicity and intact corticomedullary differentiation. Urinary myoglobin was 3,000 µg/L (reference: 0-1,000 µg/L), and serum CPK was 85,000 U/L (reference: 25-200 U/L). Total bilirubin was 1.8 mg/dL, direct bilirubin was 1.1 mg/dL, SGOT was 179 IU/L, SGPT was 1,121 IU/L, and ALP was 232 IU/L.

Figure 3. Case 2: Urine bag filled with dark-colored urine.

The investigations were suggestive of rhabdomyolysis and related complications, including AKI (KDIGO Stage III [9]) and ALI. Treatment included IV fluids, supportive measures for ALI, and hemodialysis. Hemodialysis was instituted solely as renal replacement therapy for the management of AKI and its associated metabolic complications and not for toxin removal, as para-phenylenediamine (PPD) is nondialyzable.

By the evening of Day 4, two hemodialysis sessions had been performed, and urine output increased to 500 mL/24 h. Renal and hepatic function improved, and the patient was successfully extubated. However, on Day 4, the patient developed a fever, raising suspicion of an ICU-related infection. Investigations were performed, and the results are shown in Table 3. Screening for tropical infections, including malaria parasite (ICT), dengue NS1 antigen and IgM antibody, Leptospira IgM, and scrub typhus IgM, as well as viral markers including HAV IgM and HEV IgM, was negative. Urinalysis and urine microscopy revealed no abnormalities. IV antibiotics were started after blood cultures were obtained, which later showed no growth. The fever subsided by Day 6. On Day 8, the patient was afebrile, and renal and hepatic function had returned to normal. The patient was discharged.

Table 3. Case 2: Day-wise hematological and biochemical investigations.

ALP, alkaline phosphatase; Hb, hemoglobin; PLT, platelet; SGOT, serum glutamic-oxaloacetic transaminase; SGPT, serum glutamic-pyruvic transaminase; TLC, total leukocyte count

Parameter	Day 3	Day 5	Day 6	Day 8	Reference range
TLC (/µL)	22,940	14,440	12,030	11,200	4,000-11,000
Neutrophils (%)	93.3	85	86.6	75.7	40-60
Lymphocytes (%)	3.9	12	8.21	10.8	20-40
PLT count (×10⁹/L)	282	200	231	246	150-450
Hb (g/dL)	12.8	11.3	9.7	10.2	11.0-17.0
Serum urea (mg/dL)	46	38	31	24	15-40
Serum creatinine (mg/dL)	2	1.4	1.2	1.1	0.5-1.2
Serum Na⁺ (mEq/L)	141	131	135	136	135-145
Serum K⁺ (mEq/L)	5.1	4	4.2	3.2	3.5-5.5
Total bilirubin (mg/dL)	1.4	0.9	0.7	0.7	0.3-1.3
Direct bilirubin (mg/dL)	1	0.4	0.2	0.4	0.1-0.4
SGOT (IU/L)	3,799	269	67	54	12-40
SGPT (IU/L)	1,313	1,211	345	92	8-40
ALP (IU/L)	253	218	234	211	<360

The day-wise trends in hematological, renal, and hepatic parameters are shown in Figure 4, and the overall clinical timeline is summarized in Table 4. 

Table 4. Case 2: Clinical timeline.

AKI, acute kidney injury; ALI, acute liver injury; CPK, creatine phosphokinase

Timeline	Clinical course and management
Day 0	Self-ingestion of Super Vasmol 33; presented two hours later with cervicofacial edema, stridor, hypoxemia (SpO₂ 82%), and respiratory distress. The patient was transferred to the ICU. Treatment included intramuscular adrenaline, IV hydrocortisone, chlorpheniramine, oxygen, antioxidants, and supportive care. Airway intervention was planned, and the edema improved with medical management.
Day 2	Developed oliguria with dark-colored urine. Investigations confirmed rhabdomyolysis (serum CPK 85,000 U/L; elevated urinary myoglobin) complicated by AKI and ALI. Aggressive IV fluid therapy was initiated, and hemodialysis was started.
Day 4	Two hemodialysis sessions were completed, with improvement in urine output (500 mL/24 h). The patient developed a fever, suggestive of a hospital-acquired infection. Blood cultures were obtained, and empirical antibiotics were initiated.
Day 6	The fever resolved, and blood cultures showed no growth. Renal and hepatic function improved with supportive care.
Day 8	Renal and hepatic function normalized. The patient remained afebrile and was discharged in stable condition.

Figure 4. Case 2: Day-wise trends in hematological, renal, and hepatic parameters.

(A) TLC showed a progressive decline. (B) Serum urea and serum creatinine progressively normalized, indicating recovery of renal function. (C) Liver enzymes (SGOT, SGPT, and ALP) demonstrated marked improvement during hospitalization, consistent with resolution of hepatic injury.

ALP, alkaline phosphatase; SGOT, serum glutamic-oxaloacetic transaminase; SGPT, serum glutamic-pyruvic transaminase; TLC, total leukocyte count

Discussion

Both cases illustrate poisoning complicated by rhabdomyolysis, ultimately leading to MODS. Rhabdomyolysis results from skeletal muscle injury, leading to the release of intracellular contents, including LDH, CPK, and myoglobin. It can be diagnosed by a marked elevation in CPK (>5× the upper limit of normal) in an appropriate clinical setting. Common drugs associated with rhabdomyolysis include cocaine, amphetamines, heroin, lysergic acid diethylamide, alcohol, and phencyclidine [10].

Rhabdomyolysis can cause multiorgan dysfunction, with AKI being one of the most severe complications. The proposed mechanisms of AKI in rhabdomyolysis include mechanical injury to the renal tubules due to myoglobin precipitation, direct nephrotoxicity from free chelatable iron, and hypovolemia [11]. Studies indicate that the amount of myoglobin released into the circulation correlates with serum CPK levels and the subsequent risk of AKI [12].

Beyond AKI, rhabdomyolysis can cause ALI due to hepatic ischemia and oxidative stress from free radical release. Additionally, hyperkalemia, metabolic acidosis, disseminated intravascular coagulation, and cardiac arrhythmias may occur, further contributing to MODS.

OP poisoning is defined as poisoning resulting from dermal, respiratory, or oral exposure to organophosphorus pesticides or nerve agents, leading to acetylcholinesterase (AChE) inhibition at nerve synapses [13]. This inhibition results in excessive parasympathetic activity, manifesting as bronchospasm, bronchorrhea, rhinorrhea, bradycardia, hypotension, and pinpoint pupils. Additionally, neuromuscular junction stimulation by excess acetylcholine causes fasciculations and muscle weakness.

Although rare, OP-induced rhabdomyolysis has been documented previously and is attributed to multiple mechanisms, including severe hypovolemia, prolonged seizure activity, and excessive muscular activity caused by the nicotinic effects of acetylcholine accumulation [14]. This excessive muscle activity can lead to muscle fiber breakdown, thereby increasing the risk of rhabdomyolysis and its associated complications.

The treatment of OP poisoning includes atropine, which acts as a muscarinic receptor antagonist to counteract cholinergic excess, and pralidoxime, which prevents AChE aging. According to WHO guidelines, pralidoxime is administered as a loading dose of 30 mg/kg body weight, followed by a continuous infusion at 8 mg/kg/hour. However, complications such as acute renal failure necessitate renal replacement therapy. Due to the toxicokinetic profile of OP compounds, characterized by rapid tissue distribution and a high volume of distribution, continuous veno-venous hemodialysis is preferred over conventional hemodialysis [15]. Due to the limited availability of continuous renal replacement therapy at our institution, intermittent hemodialysis was used. The patient responded favorably despite this resource limitation. The need for multiple dialysis sessions suggests severe and sustained renal injury secondary to toxin-induced rhabdomyolysis, indicating a more complicated clinical course.

In cases of ALI, supportive therapy includes N-acetylcysteine for hepatoprotection, close monitoring of coagulation parameters, and consideration of liver transplantation in cases of fulminant liver failure.

Super Vasmol 33 contains PPD, resorcinol, propylene glycol, and other ingredients [16]. PPD, an aromatic amine used for color enhancement, is the main toxic compound. It appears as white crystals that turn brown on exposure to air and is highly soluble in organic solvents. Hair dye formulations contain 2-10% PPD, with Super Vasmol containing 12 g/100 mL. The toxic dose is approximately 3 g, whereas ingestion of 7 g or more may be fatal [17].

PPD is rapidly absorbed through the mucous membranes, acetylated to N-acetyl-PPD and N,N-diacetyl-PPD, and excreted in the urine. It also forms Bandrowski’s base, a toxic and mutagenic compound. Resorcinol, a phenol derivative, is highly corrosive, whereas propylene glycol acts as a solvent. PPD, resorcinol, and propylene glycol all contribute to severe systemic toxicity [4].

PPD poisoning follows a three-stage progression [4]: (i) Initial phase (first three days): characterized by relative immunodepression due to inflammatory stress. (ii) Proinflammatory phase (Days 3-6): triggered by rhabdomyolysis, leading to systemic inflammation. (iii) Immunomodulatory phase (after Day 6): influenced by oxidative metabolism, altering immune responses.

Super Vasmol poisoning presents with a characteristic triad [18]: (A) Early angioneurotic edema: rapid swelling of the face and neck, hoarseness of voice, and stridor, often with a swollen, firm, protruding tongue and an edematous “bull neck.” (B) Rhabdomyolysis: muscle breakdown leading to dark brown urine due to myoglobinuria. (C) AKI: occurs even in the absence of preexisting renal disease, primarily due to myoglobin-induced nephrotoxicity.

Rhabdomyolysis is the main cause of renal failure and is a recognized complication of hair dye poisoning [19]. PPD causes rhabdomyolysis by promoting calcium release and leakage of calcium ions from the sarcoplasmic reticulum, followed by sustained muscle contraction and irreversible structural damage, resulting in myoglobin cast deposition within the renal tubules and hemolysis leading to acute tubular necrosis [20].

Since no antidote exists, treatment is primarily supportive, focusing on airway management, renal protection, and antioxidant therapy. Early intubation is preferred to prevent airway obstruction due to severe neck edema, whereas antihistamines and corticosteroids may help reduce allergic reactions and inflammation. Alkaline diuresis with isotonic saline, sodium bicarbonate, and osmotic diuretics is essential to prevent rhabdomyolysis-induced AKI. Although PPD is nondialyzable, hemodialysis and hemoperfusion have been attempted with mixed results [4]. Mortality depends on the dose ingested, time to intervention, and electrolyte imbalances, with reported rates of up to 60% [4].

Alternative etiologies, including traumatic muscle injury, prolonged immobilization, seizures, strenuous physical exertion, metabolic and electrolyte disturbances, infections, and concomitant use of myotoxic medications, were carefully evaluated through detailed history, clinical examination, and relevant laboratory investigations. No evidence supporting these alternative causes was identified, making acute poisoning the most likely etiology of rhabdomyolysis in both patients.

Conclusions

Rhabdomyolysis, although rare, can occur following severe acute OP poisoning and Super Vasmol poisoning. It can lead to multiorgan dysfunction and is associated with increased mortality. These two cases illustrate the diverse toxicological pathways through which muscle injury can occur, including exposure to agricultural pesticides and hair dye formulations containing PPD. In both patients, rhabdomyolysis resulted in systemic complications involving the kidneys, liver, and coagulation pathways. Serum CPK levels and renal function tests should be monitored early and serially in patients with severe poisoning, even in the absence of initial renal impairment. Aggressive fluid resuscitation, renal replacement therapy, and early airway management, particularly in hair dye poisoning, are important for improving outcomes. A high index of suspicion is therefore required for timely diagnosis and management, which may improve prognosis.