An insight into the heatstroke in Northern India: Clinico-pathological observation and outcomes from a tertiary care center

INTRODUCTION

Heatstroke is a condition of abnormal thermoregulation characterized by a fatal rise in core body temperature of more than 40°C or 104°F in addition to central nervous system abnormalities like altered consciousness, seizures, and sometimes coma along with,heatstroke can also cause multi-organ failure and death. It is a common disease that usually occurs in states with tropical climate conditions. Bundelkhand region of central India is geographically located at a place where most landscapes consist of irregular uplands with outcrops of rocks intermingling with lowlands rocky hills, and the climate is semi-arid during summers. Every year since 2010, more than 1000 deaths have been reported from various parts of India, with a maximum of 2040 deaths in 2015 and 1111 in 2016. Most of these are from Uttar Pradesh, Bihar, Maharashtra, Orissa, and Andhra Pradesh. From 2006 to 2010, more than 3332 deaths were attributed to heat-related illness.¹ Death records due to heatstroke from South Asian countries in April 2023 were 179 (India), 22 (Pakistan), 2 (Malaysia), and 2 (Thailand).

Several other infectious diseases prevalent in tropical areas of India often share common symptoms like high-grade fever, altered sensorium, and seizures. The presence of acute renal failure, rhabdomyolysis, cardiac arrhythmias, and seizures determines the high mortality rate and fatal outcomes. Effective cooling of the body and reducing core body temperature to normal without landing to hypothermia is the gold standard for the management of heatstroke. Management of hyperpyrexia or hyperthermia in the initial 24 hours of presentation to the hospital is often rewarding in cases of heatstroke. That’s why an early diagnosis and management are very important to prevent mortality and morbidities. Management of comorbidities like shock, acute renal failure, rhabdomyolysis, seizures, and multi-organ dysfunction (MODS) is done on the usual lines of treatment.

The rapid increase in the environmental temperature in the months of April and May has increased the number of cases of casualty in our Institute. In this study, we hereby present the clinical, biochemical, and treatment outcomes of the cases presented.

MATERIAL AND METHODS

RESULTS

Demography

A total of 267 patients admitted with axillary temperature ≥104°F were screened for heatstroke. After exclusion and removing who lost follow up, a total of 112 patients were enrolled for the study. Two participants with severe grades expired due to multi-organ failure. The remaining r 110 participants completed the study with no long-term morbidity.

Age is an important factor in disease severity. Figure 1 illustrates the age distribution in different severity groups. Older age is often associated with poor outcomes of acute diseases. Eighty-four (75%) participants were less than 50 years of age, out of which 71 (84.5%) developed preheatstroke, whereas 13 (15.5%) had mild to severe heatstroke. On the other hand, 28 (25%) participants were 50 years or above age, out of which nine (32.1%) developed preheatstroke and 19 (67.8%) developed mild to severe heatstroke. A chi-square test of independence showed that there was a significant association between age above 50 years and disease severity, X² (1, N = 112) = 28.2, p = 0.00001.

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Figure 1:

Flow chart of the case selection process.

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Pathological findings

All demographic, clinical, and pathological characteristics and outcomes are summarized in Table 1. A significant difference is found in three groups at the parameters of hematocrit, serum creatinine, and Blood urea Nitrogen (BUN). Figure 2 illustrates all the pathological findings among different severity groups and their frequencies.

Table 1: Clinical and pathological characteristics of participants.

Sl. No.	Characteristics	n	SD
1	Age	38.7 years	14.2
2	Sex
	Male	72
	Female	40
3	Duration of symptoms onset	23.2 hours	14.1
4	Received first aid
	Yes	91
	No	21
5	Disease severity
	Pre heatstroke	80
	Mild heatstroke	22
	Severe heatstroke	10
	• Subtype heat cramps	2
	• Subtype heat exhaustion	4
	• Subtype classical heatstroke	4
6	Axillary temperature °F (Avg.)	103	1.5
7	Pulse rate per min	139	15.9
8	Systolic BP mmHg	118	25.8
9	Diastolic BP mmHg	73.3	15.7
10	Respiratory rate per min	24	11.3
11	Clinical features n (%)
	Myalgia	28 (25.0)
	Diarrhea	13 (11.6)
	Oliguria	34 (30.5)
	Respiratory distress	9 (8.0)
	Confusion	20 (17.8)
	Delirium	3 (2.6)
	Hallucination	1 (0.8)
	Decerebrate	1 (0.8)
	Seizures	1 (0.8)
	Coma	1(0.8)
12	Pathological findings
	Hemoglobin g/dL (12–18 g%)	11.3	2.1
	Hematocrit % (36%–50%)	48.9	3.1
	Platelets count in lakh (1.5-4.5 lakh/µL)	1.3	0.4
	CRP mg/L (<0.3 mg/dL)	6.5	2.1
	IL6 pg/mL (<7 pg/mL)	24	8.6
	Creatinine mg/dL (0.7–1.3 mg/dL)	0.8	0.5
	BUN mg/dL (7–20 mg/dL)	24.7	20.4
	SGPT IL/L (19–33 IU/L)	37.9	22.6
	CPK mcg/L (10–120 mcg/L)	86.1	32.7
	RBG mg/dL (<140 mg/dl)	102.2	51.8
13	Outcome
	Survived	110
	Expired	2

CRP: C reactive Protein, IL6: Interleukin 6, BUN: Blood Urea Nitrogen, SGPT: Serum Glutamic Pyruvic transaminase, CPK: Creatine Phosphokinase, RBG: Random Blood Glucose, SD: Standard deviation.

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Figure 2:

Age distribution and disease severity.

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DISCUSSION

Heatstroke remains one of the leading causes of morbidity and mortality in summers in tropical regions in India. This study contributes several important inputs for various clinical and pathological characteristics of heatstrokes. Patients’ age always remains the most important factor for disease occurrence and disease outcomes.² In our study, out of 112 participants, 28 (25%) were ≥50 years of age. 61 ± 13.5 years was the mean age of 27 study participants in a study by Ninan et al.³ Old age is associated with less adaptive mechanisms towards heatstroke. Classical heatstroke occurs in young and old age people due to extreme heat waves during summers without preceding exertion, whereas exertional heatstroke occurs due to athletic activity or strenuous exertion during variably warm or hot weather or while wearing heat-retaining clothing.⁴ Poor sudomotor, cardiovascular, and immune function, along with defective behavioral thermoregulation, are the important factors why geriatric age is at high risk for heatstroke.⁵

Measuring rectal temperature is the best way to access the exact core body temperature during heatstroke. We lacked this in our study as we measured the axillary temperature. Axillary temperature was 103 ± 1.5°F in this study. In a study by Deshwal et al. among paratroopers suffering from exertional heat exhaustion in the Agra district of India, the average rectal temperature was 104.74°F.⁶ This is equivalent to our study considering the difference between rectal and axillary temperature, where the former remains 0.5 to 1.0°F higher than the latter.⁷ Oliguria, followed by myalgia, was the most frequent manifestation in our study. Dehydration and oliguria are present in 29% of sufferers of heatstroke.⁸ Inability to maintain hydration due to lack of water and unawareness towards heat while engaged in farm work were the common reasons due to which our study participants land up into heat-related illnesses, especially dehydration and oliguria.

Myalgia was the prominent manifestation of heatstroke presented in 28 (25%) participants. Hyponatremia and dehydration, hypokalemia, increased lactic acid levels, and exertional muscle injuries are the prominent causes of myalgia and fatigue among patients.⁹ Judicious selection of fluids, correction of electrolytes, and cold sponging are effective methods to reduce myalgia.¹⁰ The presence of confusion, mental obtundation, and restlessness are prominent features of mild and severe heatstroke.⁶ Hyponatremia, hypercalcemia, cortical vein thrombosis, lactic acidosis, and metabolic alkalosis are defined as etiological factors behind CNS manifestations of heatstroke. Further, sepsis and MODS could lead to metabolic encephalopathy and seizure.¹¹ Symptomatic management, effective cooling, and rehydration during golden hours in critical care units are always rewarding, with minimal residual CNS deformities.¹² Delirium, hallucinations, and decerebrate rigidity are also rarely reported CNS manifestations of heatstroke.^13–15 Renal dysfunction like pre-renal ARF secondary to dehydration or intrinsic renal failure due to prolonged dehydration, myoglobinuria, or sepsis syndrome is also recognized complications of heatstroke.^16,17 The average S creatinine levels in our study in the severe heatstroke group was 1.8 mg% whereas it was 0.8 mg% in pre heatstroke group. In 13 out of 112 (11.6%), S creatinine and 34 out of 112 (30.3%), BUN were more than 13 mg% and 24 mg%, respectively. The raised values of S creatinine and BUN responded to rehydration in all participants. All participants who received institutional first aid elsewhere before visiting our institute had normal renal functions clearly explains its importance. Values of other relevant investigation like Hematocrit, Platelet count, C Reactive protein, Interleukin 6, Blood urea Nitrogen, serum glutamic pyruvic transaminase (SGPT), Creatine phosphokinase and Random Blood Glucose in different severity groups are illustrated in Figure 3. Management and outcomes of participants requiring dialysis for ARF due to heatstroke are not different than the cases with other causes.¹⁸ Severe acute liver injury has also been reported due to heatstroke.¹⁹ Recognition of common pathological changes and their clinical correlation helps in management. In a study by Gharibi et al., hematocrit is raised in 87.1% of participants admitted for heatstroke.²⁰ In another study by Deshwal et al., no changes in hematocrit levels were observed during heatstroke.⁶ In our study, the significant difference in hematocrit between pre heatstroke group and the combined mild and severe group was found (t-value is –6.97367; p-value is <0.00001. The result is significant at p < 0.05). This suggests that raised hematocrit could be a predictor of poor prognosis and outcomes in heatstroke. Elevated CRP levels (152±40 mg/L) were reported by Bouchama et al. in 72% out of 28 hajj pilgrims who suffered heatstroke.²¹ IL6 was also found to be elevated and related directly to the severity of the disease in this study. In another study by Kuo-Cheng Lu et al., among participants with exertional heatstroke, proinflammatory cytokines IL-1beta, tumor necrosis factor-alpha, IL-6; T helper 1 cytokines INF-gamma and IL-2 receptor; and chemokines IL-8, monocyte chemoattractant protein 1, and Regulated upon Activation, normal T cell Expressed and Secreted (RANTES) were found to be elevated.²² CRP and IL6 levels were also elevated in this study and correlated directly with the disease severity.

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Figure 3:

Changes in pathological findings in different stages of heatstroke. (A) subject count; (B) Hematocrit; (C) Platelet count in lakh; (D) CRP; (E) IL6; (F) S. Creatinine; (G) BUN; (H) SGPT; (I) CPK; (J) RBG. Trendline denotes changes as per severity. CRP: C reactive Protein, IL6: Interleukin 6, BUN: Blood Urea Nitrogen, SGPT: Serum Glutamic Pyruvic transaminase, CPK: Creatine Phosphokinase, RBG: Random Blood Glucose.

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The biggest strength of this study is that it is the first- study done in the Bundelkhand region of India, which experiences extremes of temperature during summers and winters. The study incorporated participants suffering due to their working conditions, thus may help to add data for developing basic and advanced treatment lines for them. After searching all databases, we found that this study contributes all relevant information from the maximum number of participants ever reported from Indian studies. There are certain limitations of this study that need to be considered. First, measuring axillary temperature is not a standard method as done in this study. However, measuring oral or rectal temperature in an agitated and altered patient was not feasible. Second, a few subjects were referred to our institute after getting basic treatment. Thus, the exact clinical presentation and investigation may differ from the actual. Finally, as most of the participants were laborers working in farms and fields, thus, exactly defining the type of stroke as classical or exertional among participants was not possible.

CONCLUSION

Exposure to hot environmental temperatures can cause heatstroke with variable presentations. The outcome of heatstroke could be benign or fatal. Results from this study suggest an early and basic treatment can improve the prognosis and outcome of heatstroke. Raised hematocrit, S creatinine, and BUN suggest poor prognosis and should be managed intensively. Besides other pathological investigations, inflammatory markers like IL6 and CRP could determine prognosis in case of heatstroke. Further detailed investigatory studies are needed in critical heatstroke subjects to substantiate the observations found so far.