CME INDIA Case Presentation by Dr. N.K. Singh, MD, FICP, Director, Diabetes and Heart Research Centre, Dhanbad, Jharkhand, India. Editor, www.cmeindia.in.

CME INDIA Case Study

How Presented?

• 38 yr. old female went to market in a 3-wheeler 5 days before.
• It was intense heat. After shopping returned home but just after 5 to 6 hours, developed severe body ache and later pyrexia.
• After 3 days, developed SOB and referred to us.
• There was no history of cough or any significant prior illness.
• She got admitted on 21/06/2023.
• She was conscious, oriented, severely dyspnoeic at rest.
• Pulse-134/min.
• ECG-Sinus Tachycardia.
• Spo2-84%.
• Echo-Normal.
• USG Abdomen-Marginal Hepatomegaly, mildly prominent hepatic veins.
• CRP-32.
• ESR 31.
• TC-14,100, N81%, E 11%L07%, Platelet-2,18000/cmm.
• N/L ratio-11.5:1, Hb 11.6 gm/dl, RFT-Normal, L FT-Normal.
• D-dimer-Normal.
• NT proBNP-Normal.
• CXR-B/L Infiltrates.
• ABG-Not done as was not available.
• Blood ketone-Normal.
• CT Thorax findings:

CME INDIA Discussion

Dr. Atri Gangopadhyay, Pulmonologist, Ranchi:

• This is ARDS due to heat exhaustion.
• Although rare, but documented.
• This CT shows ARDS.
• I have come across such one case previously.
• This is basically extreme dehydration leading to cell injury.
• Management:
  • Cooling.
  • Rehydration, steroid.
  • Broad spectrum antibiotics cover.
  • Mucolytic.
  • Antioxidants.
  • Prophylactic NIV, as it avoids worsening and intubation.

Dr. S. K. Goenka, Physician, Begusarai:

• Heat exhaustion and Heat stoke are different entities. Heat stroke is a medical emergency with pt. becoming unconscious. Heat exhaustion is excessive loss of sweat due to working for much hours in heat without refuelling oneself with water/liquid.
• But it is definitely an eye opener, that Excessive heat can also cause ARDS.
• What should be the way of cooling in this patient? Because now there is ARDS.

Dr. Atri Gangopadhyay, Pulmonologist, Ranchi:

• Ice pack on body.1st infusion of cold saline, Then normal temp fluids. If body temperature normal, stop cooling.

Dr. N. K. Singh:

• Interesting. Never came across such case.

Dr. Vijaykumar P., MD, (PGI Chandigarh), DNB Medicine, Bengaluru:

• Yes, ARDS is known for Heat Stroke – overhydration, Cardiac injury, and AKD all can cause Pulmonary Oedema. Have0 seen a lot of cases in Delhi and in the Gulf. Through NGT and Rectum, I used to do Ice cold water/saline lavage to bring the Core temperature down.
• Consider rectal temperature, when available, as the most accurate measurement of core hyperthermia compared with axillary, oral, or aural thermometry.
• Do not delay initiating empiric cooling in a hyperthermic individual with an altered sensorium; cooling should not be delayed by a measurement value that may be below the diagnostic threshold of 40°C (104°F).
• Use passive cooling measures to minimize thermal strain and maximize heat loss.
• Minimize dehydration and use intravenous fluids for rehydration.
• Cold-water immersion is the optimal cooling method for heat stroke.
• Consider evaporative or convective cooling as an adjunct method if cold water immersion is unavailable. Do not use antipyretics.
• Hospital treatment:
  • Cold-water immersion should be considered for exertional heat stroke in the hospital setting.
  • One may consider evaporative and convective cooling in classic heat stroke in the hospital setting, but cooling rates with this method are inferior to those with conductive cooling.
  • Evaporative and convective cooling is not indicated in exertional heat stroke.
  • Cool heat stroke patients to a target temperature of no less than 39°C (102.2°F).
  • Give cold intravenous fluids for adjunctive cooling in heat stroke.
  • Do not use dantrolene for treating heat stroke patients. For ARDS – PEEP Ventilation.

Dated 26/06/2023

• Patient ‘all parameters – Normal.
• CT Thorax dated 26/06/2023.

Course in the hospital/ Final Diagnosis

• She was brought to our hospital with labored breathing, imaging showed lung infiltrates. She was diagnosed as a case of ARDS due to Exertional Heat Stroke. This is an extremely rare condition and CME INDIA inputs by Dr. Atri Gangopadhyay, Pulmonologist, Ranchi was vital in diagnosis and management. She was manged with non-invasive ventilation, high dose methyl prednisolone and antibiotics. No cooling methods applied as her temperature remained normal throughout. After 5th day, she improved markedly and CXR on 26^th June was normal. She was discharged on 8th day.

CME INDIA Learning Edge

• The presence of coagulopathy can play a crucial role in causing lung damage during heat stroke and serves as a reliable indicator of its occurrence. This raises the possibility of screening individuals affected by heat stroke for disseminated intravascular coagulation (DIC). By doing so, it becomes possible to identify patients who are at a higher risk of developing overt acute respiratory distress syndrome (ARDS) and enables the early implementation of measures that could potentially enhance survival rates.
• Heat stroke (HS) can manifest in two distinct clinical presentations:
• Classic HS
• Exertional HS (EHS):
  • One key distinction between classic heat stroke (HS) and exertional heat stroke (EHS) is that EHS can occur in relatively moderate climates. There have been reported cases of individuals developing EHS even at temperatures as low as 21°C (70°F). This serves as a reminder that heat-related illnesses can manifest not only in extreme environmental conditions but also in milder climates when intense physical activity is involved.
• The reason for this occurrence is primarily attributed to the combination of high environmental temperature, humidity, and strenuous exercise, leading to an elevated core body temperature. During intense physical exertion, the body generates heat, and in hot and humid conditions, it becomes challenging for the body to dissipate heat effectively. As a result, the core body temperature continues to rise, eventually leading to the development of EHS.
• It is crucial to recognize that individuals engaging in physical activities, such as sports, labor-intensive work, or recreational activities, in relatively moderate climates still face the risk of EHS. Proper precautions, such as staying hydrated, taking frequent breaks in shaded or cooler areas, and monitoring one’s body for signs of heat exhaustion or heat stroke, should be taken to prevent heat-related illnesses, even in milder climates.

Characteristics of classical and exertional heat stroke

Characteristics Classical Heat Stroke

• Age group – Older.
• Occurrence – Epidemic.
• Predisposing illness – Frequent.
• Weather – Heat wave.
• Scene-Indoor (incidence increases greatly during a heat wave).
• Time to onset – Gradual deterioration over days.Acid-base status – Respiratory alkalosis.
• Rhabdomyolysis, renal failure, DIC-Rare.
• Hyperuricemia – Mild.
• Prognosis – Bad.

Characteristics of Exertional Heat Stroke

• Age group – Young.
• Occurrence – Sporadic.
• Scene outdoors, under a hot sun.
• Time to onset -Sudden onset within a few hours.
• Predisposing illness – Rare.
• Weather – Variable.
• Acid-base status- Respiratory alkalosis + lactic acidosis.
• Rhabdomyolysis, renal failure, DIC-Common.
• Hyperuricemia – Marked.
• Prognosis – Good.

• Progression to acute respiratory distress syndrome (ARDS) occurs due to hyperventilation and pulmonary vasodilation and hyperpermeability due to hyperpnea and cytokines.
• Baseline tests for evaluating a patient suspected of a medical condition or illness should encompass several diagnostic procedures.
• The AECC defined ARDS as an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary oedema. The severity of hypoxemia necessary to make the diagnosis of ARDS was defined by the ratio of the partial pressure of oxygen in the patient’s arterial blood (PaO₂) to the fraction of oxygen in the inspired air (FiO₂). ARDS was defined by a PaO₂/FiO₂ ratio of less than 200, and in ALI, less than 300.
• Base line CXR could be vital. The pulmonary infiltrates usually evolve rapidly, with maximal severity within the first 3 days. Infiltrates can be noted on chest radiographs almost immediately after the onset of gas exchange abnormalities. They may be interstitial, characterized by alveolar filling, or both.
• Initially, the infiltrates may have a patchy peripheral distribution, but soon they progress to diffuse bilateral involvement with ground glass changes or frank alveolar infiltrates
• This imaging technique helps assess the condition of the lungs and chest cavity, aiding in the identification of potential abnormalities.
• Lab Tests Needed:
  • ECG (Electrocardiogram.
  • Cardiac enzymes.
  • Arterial blood gas study.
  • Blood tests for malarial parasite.
  • Prothrombin time and fibrinogen level: These tests evaluate the blood’s ability to clot properly and assess the functioning of the coagulation system.
  • Blood chemistry profile: This includes a comprehensive panel of blood tests that measure various substances, such as electrolytes, liver enzymes, kidney function markers, and glucose levels, providing an overview of the patient’s overall health.
  • Creatine kinase (CK) It can be useful in assessing if there has been muscle injury or breakdown.
  • Urinalysis, including urine for myoglobin: Urine analysis helps evaluate kidney function and the presence of any abnormal substances. In the context of heat stroke or muscle injury, testing for myoglobin in the urine can indicate muscle breakdown.
• Management: Although no specific therapy exists for ARDS, treatment of the underlying condition is essential, along with supportive care, non-invasive ventilation or mechanical ventilation using low tidal volumes, and conservative fluid management. Because infection is often the underlying cause of ARDS, early administration of appropriate antibiotic therapy broad enough to cover suspected pathogens is essential.
• Although no survival advantage was shown in patients treated with methylprednisolone, short-term clinical benefits included improved oxygenation and increased ventilator-free and shock-free days.

CME INDIA Tail Piece

Courtesy: Hifumi, T., Kondo, Y., Shimizu, K. et al. Heat stroke. j intensive care 6, 30 (2018). https://doi.org/10.1186/s40560-018-0298-4

References:

1. Hifumi, T., Kondo, Y., Shimizu, K. et al. Heat stroke. j intensive care 6, 30 (2018). https://doi.org/10.1186/s40560-018-0298-4
2. el-Kassimi FA, Al-Mashhadani S, Abdullah AK, Akhtar J. Adult respiratory distress syndrome and disseminated intravascular coagulation complicating heat stroke. Chest. 1986 Oct;90(4):571-4. doi: 10.1378/chest.90.4.571. PMID: 3757568.
3. Mehta SR, Jaswal DS. Heat Stroke. Med J Armed Forces India. 2003 Apr;59(2):140-3. doi: 10.1016/S0377-1237(03)80062-X. Epub 2011 Jul 21. PMID: 27407489; PMCID: PMC4923787.
4. Giercksky T, Boberg KM, Farstad IN, Halvorsen S, Schrumpf E. Severe liver failure in exertional heat stroke. Scand J Gastroenterol 1999;8:824-7.
5. Mehta SR, Narayanaswamy AS. Heat stroke. J Assoc Phy India.1987;35:822-5
6. Castillo OG, Solís C. Pulmonary hemorrhage and acute respiratory distress syndrome secondary to heat stroke. Rev Inst Nal Enf Resp Mex. 2006;19(4):276-281.
7. https://www.med.or.jp/english/journal/pdf/2013_03/167_173.pdf

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