Dr Puneet Kumar Misra
Abstract
Key notes materia medica to guiding symptoms materia medica describe the glonoinum as a very important medicine in respect of heat disorder from initially to ultimate. In the clinical practice when the disorder associated with the heat or high surrounding temperature the most of the practitioners start of choice in treatment is glonoinum and this remedy never fail to start the improve the human health .
Introduction – Human body is very sensitive with the alteration of the surrounding temperature and it respond in different way to depth of effect . the high temperature or heat are effect all system of body or organ , initially heat effect with some non specific disorder like limb swelling ,muscle spasm , thirst, lethargy, headache, nausea, coarse muscle tremor, confusion, aggression and loss of consciousness with or without sweating till heat stroke .
Heat oedema – Mild swelling to the limbs during the first few days of heat exposure due to increased plasma volume, peripheral vasodilation and interstitial pooling of blood.1
Heat cramps – Muscle spasms related to sodium loss. Generally occur after exercise in non-acclimatised individuals who sweat freely and replace losses with water or other hypotonic solutions, so they become salt depleted. Salt supplementation reduces the incidence.1
Heat syncope – Heat syncope refers to a multi-factorial syndrome involving transient loss of consciousness in the context of heat exposure with a relatively rapid return to normal function and baseline. Contributing factors may include peripheral vasodilation, orthostatic pooling of blood, prolonged standing, advanced age and dehydration, as well as coexisting medical conditions such as ischaemic heart disease that reduce cardiac output.1
Heat exhaustion – Characterized by volume and salt depletion. It is an inability to continue an activity due to heat stress. It presents with thirst, lethargy, headache, nausea but importantly a normal mental status. Some literature describes it as benign as it may be protective in the development of heat stroke, causing an individual to stop an activity and thus the generation of heat.1
Heat stroke – Neurological impairment with core body temperature ≥40°C (rectal temperature is gold standard in a pre-hospital environment). Symptoms can involve a coarse muscle tremor, confusion, aggression and loss of consciousness. Sweating may be absent due to dehydration and failure of thermoregulatory mechanisms.1
Pathophysiology of heat stroke – The heat stroke can be summarized as organ dysfunction from the high temperature itself, and end-organ ischemia from diminished blood flow. Increased sweating results in dehydration and blood pools in vasodilated peripheral vasculature resulting in a decreased effective blood volume. The blood viscosity increases resulting in heart strain. Enzymes denature at 40 °C and at 41 °C mitochondrial activity stops; the subsequent loss of oxidative phosphorylation results in organ ischaemia. The muscles and gastrointestinal tract are affected first, followed by the central nervous system, circulatory and clotting systems. The pathophysiology is similar to sepsis, severe trauma and extensive burns.1
FACTORS PREDISPOSING TO SERIOUS HEAT ILLNESS
INDIVIDUAL FACTORS – Lack of acclimatization, Low physical fitness. Excessive body weight ,Dehydration, Advanced age, Young age, Toll-like receptor-4 polymorphisms.2
HEALTH CONDITIONS – Inflammation and fever, Viral or bacterial infection, Cardiovascular disease, Diabetes mellitus ,Gastroenteritis ,Rash, sunburn, and previous burns to large areas of skin, Seizures Thyroid storm, Neuroleptic malignant syndrome, Malignant hyperthermia, Sickle cell trait ,Cystic fibrosis.2
ENVIRONMENTAL FACTORS – High temperature High humidity little air motion Lack of shade Heat wave Physical exercise Heavy clothing Prior compromised heat exposures .2
Heat illness accounts for considerable morbidity and mortality in the world today. Serious heat illness is associated with a variety of individual factors, health conditions, drugs, and environmental factors. Exertional heat illness is among the leading causes of death in young athletes, and its incidence appears to be increasing in the United States. Classic heat illness caused by high environmental temperatures remains a problem especially in homebound elderly persons without air conditioners.2 Anticholinergic and sympathomimetic poisoning can induce hyperthermia. Malignant hyperthermia is a rare disorder occurring in genetically predisposed individuals. Rapid and massive skeletal muscle contraction from exposure to certain volatile anesthetic agents (most commonly halothane, sevoflurane, desflurane, isoflurane, or enflurane) or depolarizing muscle agents relaxants (e.g., succinylcholine) can trigger core temperature elevations well above 43° C (110° F). However, some data suggest that heat disorders with extreme exercise may represent a similar syndrome.3 Neuroleptic malignant syndrome is an idiosyncratic hyperthermic reaction caused by skeletal muscle rigidity from treatment with neuroleptic medications (e.g., antipsychotics, antidepressants, antiemetics). Both malignant hyperthermia and neuroleptic malignant syndrome are potentially fatal without prompt recognition and early intervention. Heat illness can also occur in low-risk individuals who have taken appropriate precautions relative to situations to which they have been exposed in the past. Historically, such unexpected cases were attributed to dehydration (which impairs thermoregulation and increases hyperthermia and cardiovascular strain), but it is now suspected that a previous heat exposure or a concurrent event (e.g., sickness or injury) might make these individuals more susceptible to serious heat illness. One theory is that previous heat injury or illness primes the acute phase response and augments the hyperthermia of exercise, inducing unexpected serious heat illness. Another theory is that previous infection produces proinflammatory cytokines that deactivate the cells’ ability to protect against heat shock.2
PATHOBIOLOGY Body temperature can increase from a number of mechanisms: exposure to environmental heat (impeded heat dissipation); physical exercise (increased heat production); fever from systemic illness (elevated set point with subsequent activation of shivering); and medications (neuroleptic malignant syndrome and malignant hyperthermia). In addition, febrile persons have accentuated elevations in core temperature when they are exposed to high ambient temperature, physical exercise, or both. Environmental temperature and humidity, medications, and exercise heat stress in turn challenge the cardiovascular system to provide high blood flow to the skin, where blood pools in warm, compliant vessels such as those found in the extremities. When blood flow is diverted to the skin, reduced perfusion of the intestines and other viscera can result in ischemia, endotoxemia, and oxidative stress. Several common mutations in toll-like receptor 4 are associated with endotoxin hyporesponsiveness. In addition, excessively high tissue temperatures (heat shock: >41° C [105.8° F]) can produce direct tissue injury; the magnitude and duration of the heat shock influence whether cells respond by adaptation (acquired thermal tolerance), injury, or death (apoptotic or necrotic). Heat shock, ischemia, and systemic inflammatory responses can result in cellular dysfunction, disseminated intravascular coagulation, and multiorgan dysfunction syndrome. Furthermore, reduced cerebral blood flow, combined with abnormal local metabolism and coagulopathy, can lead to dysfunction of the central nervous system.2
CLINICAL MANIFESTATIONS AND DIAGNOSIS Minor heat illness is common and can be recognized by its clinical features. Miliaria rubra (heat rash) results from the occlusion of eccrine sweat gland ducts and can be complicated by secondary staphylococcal infection. Heat syncope (fainting) is caused by temporary circulatory insufficiency as a result of blood pooling in the peripheral veins, especially the cutaneous and lower extremity veins. Skeletal muscle cramps most commonly occur during and after intense exercise and are probably related to dehydration, loss of sodium or potassium, and neurogenic fatigue rather than to overheating itself. Serious heat illness includes heat exhaustion, heat injury, and heatstroke, with some individuals progressing along this spectrum. Patients who exhibit symptoms (e.g., dizziness, un-steady gait, ataxia, headache, confusion, weakness, fatigue, nausea, vomiting, diarrhea) should have an immediate assessment of their mental status, core (rectal) temperature, and other vital signs. The most common causes of hospital admission are fluid and electrolyte disorders, renal failure, urinary tract infection, and heatstroke. Until proven otherwise, heatstroke should be the initial working diagnosis in anyone who is a heat casualty and has an altered mental status. 2
Heat exhaustion is defined as a syndrome of hyperthermia (temperature at time of event usually ≤40° C or 104° F) and debilitation that occur during or immediately after exertion in the heat, accompanied by no more than minor central nervous system dysfunction (headache, dizziness, mild confusion), which resolves rapidly with intervention. It is primarily a cardiovascular event (insufficient cardiac output) frequently accompanied by sweaty hot skin, dehydration, and collapse. 2
Heat injury is a moderate to severe illness characterized by evidence of damage to end organs (e.g., liver, renal, gut) and tissues (e.g., rhabdomyolysis) without sufficient neurologic symptoms to be diagnosed as heatstroke. It is usually associated with body temperatures above 40° C (104° F).2 Heatstroke is a severe illness characterized by profound mental status changes with high body temperatures, usually but not always higher than 40° C (104° F). However, patients with a core temperature higher than 40° C do not universally have a heat injury or heatstroke, and core temperatures this high can be seen transiently after stressful exercise in the heat. To establish the diagnosis of heatstroke, the entire clinical picture, including mental status and laboratory results, must be considered. Heatstroke is often categorized as classic or exertional; classic heatstroke is observed primarily in otherwise sick and compromised individuals, and exertional heatstroke is observed primarily in apparently healthy and physically fit individuals during or after vigorous exercise. In heatstroke, neuropsychiatric impairments (e.g., marked confusion, disorientation, combativeness, and seizures) develop early and universally but are readily reversible with early cooling. In addition, heatstroke can be complicated by liver damage, rhabdomyolysis, disseminated intravascular coagulation, water and electrolyte imbalance, and renal failure. In fulminant heatstroke, patients have the full spectrum of abnormalities associated with the systemic inflammatory response syndrome . 2
MANAGEMENT OF HEAT ILLNESS
HEAT EXHAUSTION Rest and shade Loosen and remove clothing Supine position and elevate legs Actively cool skin Fluids by mouth Monitor core temperature Monitor mental status
HYPERTHERMIA– Protect the airway Insert at least two large-bore intravenous lines Monitor core temperature; options include rectal, pulmonary artery, esophageal probe Actively cool the skin until core temperature reaches<39 C(<102.2F) .Ice baths or cool water (≈22° C [71.6° F]) immersion Wetting with water (avoid alcohol rubs) Continuous fanning Exposure to cool environment Axillary or perineal ice packs and ice sheets Infusion of room-temperature saline Gastric or colonic iced saline lavage Peritoneal lavage with cool saline Monitor electrocardiogram for arrhythmia Obtain serial diagnostic studies* 2
Heat-related illnesses include a spectrum of disorders ranging from heat syncope, muscle cramps, and heat exhaustion to medical emergencies such as heatstroke. The core body temperature is normally maintained within a very narrow range. Although significant levels of hypothermia are tolerated, multiorgan dysfunction occurs rapidly at temperatures >41°–43°C.3
THERMOREGULATION Humans are capable of significant heat generation. Strenuous exercise can increase heat generation twentyfold. The heat load from metabolic heat production and environmental heat absorption is balanced by a variety of heat dissipation mechanisms. These central integrative dissipation pathways are orchestrated by the central thermostat, which is located in the preoptic nucleus of the anterior hypothalamus. Efferent signals sent via the autonomic nervous system trigger cutaneous vasodilation and diaphoresis to facilitate heat loss. Normally, the body dissipates heat into the environment via four mechanisms. The evaporation of skin moisture is the single most efficient mechanism of heat loss but becomes progressively ineffective as the relative humidity rises to >70%. The radiation of infrared electromagnetic energy directly into the surrounding environment occurs continuously. (Conversely, radiation is a major source of heat gain in hot climates.) Conduction—the direct transfer of heat to a cooler object— and convection—the loss of heat to air currents—become ineffective when the environmental temperature exceeds the skin temperature. Factors that interfere with the evaporation of diaphoresis significantly increase the risk of heat illness. Examples include dripping of sweat off the skin, constrictive or occlusive clothing, dehydration, and excessive humidity. While air is an effective insulator, the thermal conductivity of water is 25 times greater than that of air at the same temperature. more common sign of fever reflects intact thermoregulation. The wet-bulb globe temperature is a commonly used index to assess the environmental heat load. This calculation considers the ambient air temperature, the relative humidity, and the degree of radiant heat. The regulation of this heat load is complex and involves the central nervous system (CNS), thermosensors, and thermoregulatory effectors. The central thermostat activates the effectors that produce peripheral vasodilation and sweating.
The skin surface is in effect the radiator and the principal location of heat loss, since skin blood flow can increase 25–30 times over the basal rate. This dramatic increase in skin blood flow, coupled with the maintenance of peripheral vasodilation, efficiently radiates heat. At the same time, there is a compensatory vasoconstriction of the splanchnic and renal beds. Acclimatization to heat reflects a constellation of physiologic adaptations that permit the body to lose heat more efficiently. This process often requires one to several weeks of exposure and work in a hot environment. During acclimatization, the thermoregulatory set point is altered, and this alteration affects the onset, volume, and content of diaphoresis. The threshold for the initiation of sweating is lowered, and the amount of sweat increases, with a lowered salt concentration. Sweating rates can be 1–2 L/h in acclimated individuals during heat stress. Plasma volume expansion also occurs and improves cutaneous vascular flow. The heart rate lowers, with a higher stroke volume. After the individual leaves the hot environment, improved tolerance to heat stress dissipates rapidly, the plasma volume decreases, and deacclimatization occurs within weeks.3
PREDISPOSING FACTORS AND DIFFERENTIAL DIAGNOSIS – When there is an excessive heat load, unacclimated individuals can develop a variety of heat-related illnesses. Heat waves exacerbate the mortality rate, particularly among the elderly and among persons lacking adequate nutrition and access to air-conditioned environments. Secondary vascular events, including cerebrovascular accidents and myocardial infarctions, occur at least 10 times more often in conditions of extreme heat. Exertional heat illness continues to occur when laborers, military personnel, or athletes exercise strenuously in the heat. In addition to the very young and very old, preadolescents and teenagers are at risk since they may use poor judgment when vigorously exercising in high humidity and heat. Other risk factors include obesity, poor conditioning with lack of acclimatization, and mild dehydration. Cardiovascular inefficiency is a common feature of heat illness. Any physiologic or pharmacologic impediment to cutaneous perfusion impairs heat loss. Many patients are unaware of the heat risk associated with their medications. Anticholinergic agents impair sweating and blunt the normal cardiovascular response to heat. Phenothiazines and heterocyclic antidepressants also have anticholinergic properties that interfere with the function of the preoptic nucleus of the anterior hypothalamus due to central depletion of dopamine.
Calcium channel blockers, beta blockers, and various stimulants also inhibit sweating by reducing peripheral blood flow. To maintain the mean arterial blood pressure, increased cardiac output must be capable of compensating for progressive dehydration. A variety of stimulants and substances of abuse also increase muscle activity and heat production. Careful consideration of the differential diagnosis is important in the evaluation of a patient for a potential heat-related illness. The clinical setting may suggest other etiologies, such as malignant hyperthermia after general anesthesia. Neuroleptic malignant syndrome can be triggered by certain antipsychotic medications, including selective serotonin reuptake inhibitors. A variety of infectious and endocrine disorders as well as toxicologic or CNS etiologies may mimic heatstroke .3
MINOR HEAT-EMERGENCY SYNDROMES
Heat edema is characterized by mild swelling of the hands, feet, and ankles during the first few days of significant heat exposure. The principal mechanism involves cutaneous vasodilation and pooling of interstitial fluid in response to heat stress. Heat also increases the secretion of antidiuretic hormone and aldosterone. Systemic causes of edema, including cirrhosis, nephrotic syndrome, and congestive heart failure, can usually be excluded by the history and physical examination. Heat edema generally resolves without treatment in several days. Simple leg elevation or compression stockings will usually suffice. Diuretics are not effective and, in fact, predispose to volume depletion and the development of more serious heat-related illnesses. Prickly heat (miliaria rubra, lichen tropicus) is a maculopapular, pruritic, erythematous rash that commonly occurs in clothed areas. Blockage of the sweat pores by debris from macerated stratum corneum causes inflammation in the sweat ducts. As the ducts dilate, they rupture and produce superficial vesicles. The predominant symptom is pruritus. In addition to antihistamines, chlorhexidine in a light cream or lotion provides some relief. In adults, localized areas may benefit from 1% salicylic acid TID, with caution taken to avoid salicylate intoxication. Clothing with breathable fabric should be clean and loose fitting, and activities or environments that induce diaphoresis should be avoided. Heat syncope (exercise-associated collapse) can follow endurance exercise or occur in the elderly. Other common clinical scenarios include prolonged standing while stationary in the heat and sudden standing after prolonged exposure to heat. Heat stress routinely causes relative volume depletion, decreased vasomotor tone, and peripheral vasodilation. The cumulative effect of this decrease in venous return is postural hypotension, especially in nonacclimated elderly individuals. Many of those affected also have comorbidities. Therefore, other cardiovascular, neurologic, and metabolic causes of syncope should be considered. After removal from the heat source, most patients will recover promptly with cooling and rehydration. Hyperventilation tetany occurs in some individuals when exposure to heat stimulates hyperventilation, producing respiratory alkalosis, paresthesia, and carpopedal spasm. Unlike heat cramps, heat tetany causes very little muscle-compartment pain. Treatment includes providing reassurance, moving the patient out of the heat, and addressing the hyperventilation 3
COOLING STRATEGIES
Before cooling is initiated, endotracheal intubation and continuous core-temperature monitoring should be considered. Peripheral methods to measure temperature are not reliable. Hypoglycemia is a frequent finding and can be addressed by glucose infusion. Since peripheral vasoconstriction delays heat dissipation, repeated administration of discrete boluses of isotonic crystalloid for hypotension is preferable to the administration of α-adrenergic agonists. Evaporative cooling is frequently the most practical and effective technique. Rapid cooling is essential in both CHS and EHS, and an immediate improvement in vital signs and mental status may prove valuable for diagnostic purposes. Cool water (15°C [60°F]) is sprayed on the exposed skin while fans direct continuous airflow over the moistened skin. Cold packs applied to the neck, axillae, and groins are useful cooling adjuncts. If cardiac electrodes will not adhere, they can be applied to the patient’s back. Immersion cooling in ice-cold water is an alternative option in EHS but can induce peripheral vasoconstriction and shivering. The initial increase in temperature from peripheral vasoconstriction will rapidly be overcome by the large conductive thermal transfer into cold water. This technique presents significant monitoring and resuscitation challenges in many clinical settings. The safety of immersion cooling is best established for young, previously healthy patients with EHS (but not for those with CHS). To avoid hypothermic after drop (continued cooling after immersion), active cooling should be terminated at ~38°–39°C (100.4°F–102.2°F). Cooling with commercially available cooling blankets should not be the sole technique used, since the rate of cooling is far too slow. Other methods are less efficacious and rarely indicated, such as IV infusion of cold fluids and cold irrigation of the bladder or gastrointestinal tract. Cold thoracic and peritoneal lavages is efficient maneuvers but are invasive and rarely necessary. Endovascular cooling also provides effective cooling 3
DISPOSITION Most patients with minor heat-emergency syndromes (including heat edema, heat syncope, and heat cramps) require only stabilization and treatment with outpatient follow-up. Although there are no decision rules to guide disposition choices in heat exhaustion, many of these patients have multiple predisposing factors and co morbidities that will require prolonged observation or hospital admission. Essentially all patients with actual heatstroke require admission to a monitored setting, and most require intensive care. There are reports of very high survival rates of patients following pre hospital immersion cooling without intensive care. Most or all of these patients appear to have had heat exhaustion. Many actual heatstroke patients also require prolonged tracheal intubation, invasive hemodynamic monitoring, and support for various degrees of multi organ dysfunction syndrome. The prognosis worsens if the initial core temperature exceeds 42°C (107.6°F) or if there was a prolonged period during which the core temperature exceeded this level. Other features of a negative prognosis include acute renal failure, massively elevated liver enzymes, and significant hyperkalemia. As expected, the number of dysfunctional organ systems also correlates directly with mortality risk.3
Matriea medica view
- Head troubles: from working under gas-light, when heat falls on head; cannot bear heat about the head, heat of stove or walking in the sun [Lach. , Nat. c.]. Cerebral congestion or alternate congestion of the head and heart. Head: feels enormously large; as if skull were too small for brain; sunstroke and sun headache; increases and decreases every day with the sun [Kal. , c. ]. Terrific shock in the head, synchronous with the pulse.4
- #Head CONFUSION, with dizziness. Effects of sunstroke; heat on head, as in type-setters and workers under gas and electric light. HEAD HEAVY, BUT CANNOT LAY IT ON PILLOW. CANNOT BEAR ANY HEAT ABOUT HEAD. Better from uncovering head. THROBBING headache. Angio-spastic neuralgia of head and face. Very irritable. Vertigo on assuming upright position. Cerebral congestion. Head feels enormously large, as if skull were too small for brain. Sun headaches; increases and decreases with the sun. Shocks in head, synchronous with pulse.5
- #Modalities BETTER, brandy. WORSE, in sun; exposure to sun-rays, gas, open fire; jar, stooping, having hair cut; peaches, stimulants; lying down; from 6 a.m. to noon; left side .5
- #Causation Sun. Bright snow. Fire-heat. Fear or fright. Jarring. Injuries.6
- #Head – Vertigo, worse from stooping or moving head, in open air. Giddiness when the head is moved. Heaviness in the head, principally in forehead. Dull headache with warm perspiration on forehead. Headache with accelerated pulse, red face, perspiration on the face, he becomes unconscious. Headache worse from the heat of the sun, better in the open air and from pressure.6
- #Face Paleness of the face with heat and congestion of blood to head and chest. Pale during heat, sunstroke, congestions, , flushed and hot with headache.6
- #Heart – Pulse accelerated, rises and falls alternately, low and feeble in sunstroke .6
- #Fever Pulse accelerated, irregular, intermitting, full and hard, small and rapid. Chill: after getting heated, alternates with sweat, with vomiting, head as if screwed up, intermittent fever. 6
- #Temperature and Weather -Children get sick in the night after sitting opposite an open. coal fire, or falling asleep there. Bad effects from having the hair cut. Bad effects from being exposed inordinately to the sun’s rays. Open air: vertigo Agg.; headache with unconsciousness Amel. Damp, rainy days: headache. Wet, dull weather: attacks of headache. Gas-light: causes headache. Warm weather: brings back headache. Warm room: headache Agg. Heat of bed: Faceache Agg. Taking cold from overheating: cause headache. Overheating: causes headache. Hot applications: Agg. pain in gums. Heat: head will not bear it. Cannot walk in sun nor bear heat from stove. Rays of sun cannot be borne on head. Bad result from sunstroke. Cold applications: Amel. pains in gums. Cold air: Amel. headache. Cold water: headache; cause spasms; Amel. Congestive headache. Excessive cold and heat: cause hyperaemia of brain.7
- #Attacks Periodicity Gradually: headache growing more severe after working in sun. Periodical attacks: of facial neuralgia.7
- #Tissues Bad effects from mental excitement, fright, fear, mechanical contusions and their later consequences, from having hair cut and exposure to rays of sun.7
- Have I not described to a great extent that which is seen in a typical sunstroke? It is noticeable also that Glonoine symptoms are worse in the heat of summer and relieved in winter. The dull headaches and the continuous headaches are aggravated from warm weather and ameliorated from cold. They are worse in the sun and better in the shade. .All sorts of contrivances will be resorted to by Glonoine patients to keep the suns heat from the head. When he has had these troubles for years, and it has become a chronic state he will never go out in the warmth of the sun without an 8
- Sudden local congestion, especially to head and chest; bursting headache rising up from neck, with great throbbing and sense of expansion as if to burst; cannot bear the least jar,Can’t bear anything on the head, especially hat; or pressure as of a hat. Over-heating in the sun, or sunstroke. For sunstroke it is probably oftener indicated than any other remedy; also for the after-sufferings therefrom. Not only from sunstroke, but from the other bad effects of RADIATE HEAT; 9
The study on the Glonoinum are focused on the mentioned disorder in the table 01 and Continues observation of drug action on more than five years and 87 case found during study (State Pt J L N Homoeopathy medical college and hospital Kanpur) details are given in table 02.
Table 01
| S.No | Disorder | Observation |
| 01 | Headache in summar weather | Good response |
| 02 | Burning or mild pain of lower extremities summar weather | Marked response |
| 03 | Lethargic with headache and perspiration with thirst | Moderate effect |
| 04 | Lethargic with headache and no perspiration no thirst | Marked effect |
| 05 | Lethargic with headache and cramp in lower limbs | Mild to Moderate |
| 06 | Facial eruption with dryness in summar without other complain | Mild to Moderate |
Table 02
| TOTEL CASE | 87 | MALE | 45 | FEMALE | 42 |
Table 03
| Age group distribution in Years | ||||||||
|
Discussion
1 – Commonly heat related disorders are not come regularly because the heat related disorder highly affected by environment and surrounding temperature its usual onset from April and end in July till heat wave .
2 – As per above details the heated related disorders clinically present with some non specifics complain , therefore after complete history it decide that the non specifics complain is due to the heat related .
3 – Treatment of the heat related disorder is based on its clinical manifestations i.e. minor central nervous system dysfunction (headache, dizziness, mild confusion), which resolves rapidly and heatstroke can be complicated by liver damage, rhabdomyolysis, disseminated intravascular coagulation, water and electrolyte imbalance, and renal failure.
4 – Most of the patients age between 15 to 55 years and 30c and 1m found un effective in single as well as repeated dose while 200c found much effective in the repeated dose with cooling and rehydration management .In mild to moderate case the improvement start within 6 to 8 hours with repeated dose in 4-6 hours
5 – At initial stage of treatment minor central nervous system dysfunction start to resolves within 8-12 hours but failure of cooling and rehydration management the amelioration stop there for during treatment focus on the all points.
6- this medicine is an emergency medicine and need of it continues use up to full recovery . Once complete recovery no need of treatment.
Conclusion – Glonoinum is the well indicated and suitable medicine for the treatment of heat associated disorder when apply it in the proper manner as per manifestations of the disorder with all essential management measures during recovery of the illness.
Reference
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Dr Puneet Kumar Misra
Reder (Practice of Medicine)
Govt L B S H M C Prayagraj
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