Shock; when this term is used by physicians it indicates of a medical disorder, in fact a serious one that is the consequence of widespread & imperfect perfusion of the body cells.

The body cells are dependent upon a constant supply of blood to meet their need for oxygen, fuels & other nutrients. If for any reason this blood supply becomes critically inadequate and also happens diffusely in the body then the out come is a state of shock.

Please note that this term is not equivalent with the general non-medical term shock which usually connotes of a traumatic emotional experience.

Types/ Classification of shock

The following are the types of shock;

* Hypovolemic (decreased blood volume)
* Traumatic
* Heart related (cardiogenic)

Intrinsic
Compressive

* Neurogenic
* Septic

Hyperdynamic
Hypodynamic

* Hypoadrenal (adrenal gland related)

Hypovolemic shock: This is the most common form of shock and results from severe blood loss or fluid loss in the form of vomiting, diarrhea, excessive urine out put etc. Patient’s lips, mouth are dry, skin loses its turgor and veins are collapsed.

Cardiogenic shock: This results due to conditions like major heart attack. Here actually the total body fluid content is not subnormal rather blood pools in the venous bed due to heart’s inability to pump it into the arteriolar circulation. Patient’s do not appear dry and also their veins are not collapsed rather may look more prominent.

Traumatic shock is mostly due to blood loss and hypovolemia but there is usually more that that. Due to the injury certain inflammatory substances promote the loss of plasma from the vessels in to the interstitium. The clinical manifestations in generally resemble the hypovolemic shock.

Neurogenic shock: This generally occurs during a high level (neck level) spinal cod injury and resulting hypo-functioning of adrenergic response. These patents do not appear dry and their veins are generally not collapsed.

Hypo adrenergic shock: When body is encountered with stress the adrenal gland hyper secrete cortisol (glucocoticoid) to withstand the stress as much as possible. However due to any adrenal hypo-functioning during stressful situations cortisol secretion is not adequate and this will result in shock.

What causes shock?

When acute & severe circulatory failure happens the body cells are deprived of their oxygen and other nutrition and result in cellular dysfunction. This cellular injury induces the production of what are called as inflammatory mediators and these substances further compromise the circulation of blood through what is called as microvasculature. The outcome of this is a vicious cycle during which the diminished blood flow results in cellular injury and the response of injured cells results in decreased perfusion and this can continue on and on until severe and irreversible damage to multiple body organs may take place and eventual death.

How do the different tissues & organs respond to shock?

Neuroendocrine response:

The decreased blood volume, blood pressure and oxygen concentration in the blood activate systems called as baroreceptos & chemoreceptors which in turn increase adrenergic activity and suppresses parasympathetic & vagal activities. The stress and pain induces the secretion of steroids (glucocorticoids)  and the out come of these various activities is to increase the blood sugar, cut down on blood flow to non vital organs like skin, gastrointestinal tract etc and optimize blood low to vital organs like brain, heart etc.

Cardiovascular response:

Unless the heart is injured and itself caused the shock (cardiogenic shock) the response of heart to shock is by beating faster & stronger mainly due to increased sympathetic (adrenergic type) activity so that the blood volume can be restored. The increased adrenergic activity also causes narrowing of the venous blood vessels and augments the return of blood to the heart and facilitates its pumping from the heart.

Kidney response:

Kidneys try to reduce urine out put so as to restore the blood volume. Kidneys also release an enzyme called as renin that cleaves a substance by name angiotensin I from a protein substrate. Angiotensin I in turn is converted to angiotensin II in the lungs. Angiotensin II is a powerful constrictor of blood vessels and also it stimulates the release of a hormone by name aldosterone from the adrenal glands. Both angiotensin II and aldosterone try to elevate the blood pressure.

Metabolic response:

The severe decreased perfusion and resultant diminished fuel supply forces the body cells to look for alternate source. As mentioned above the adrenergic, steroid hormones make more glucose available although to use it efficiently the cells need oxygen which is limiting. So cells resort for alternate but less efficient means of utilization of glucose called anaerobic pathways and a substance called as lactate is produced in the process. If too much of lactate accumulates it can increase the acidity of the blood and contribute for additional cell damage.

Lung response:

The lungs try to compensate for diminished oxygen in the blood by increasing the breathing rate. A condition called as respiratory alkalosis can result due to rapid breathing. Shock can also result in a severe form of lung injury called as ARDS (acute respiratory distress syndrome).

Diagnosis

The diagnosis of shock is mostly a clinical one although several investigations are required to identify the cause of shock.

The following are certain characteristic clinical manifestation that would help in identifying the shock;

* Severe low blood pressure (generally <60 mmHg mean arterial pressure)
* Patient either comatose or with decreased level of consciousness
* Decreased urine out put of varying grades

The following investigations or procedures are generally necessary in the diagnosis & management of shock including;

* Blood tests
* Urine analysis
* Imaging studies
* Any special tests (e.g. biopsy) etc.

A complete blood count may show anemia indicating blood loss, increased white blood cells indicating infection etc. Electrolyte analysis may reveal abnormalities that might hint blood concentration, kidney dys-functioning etc.

Imaging studies including U/S, Echocardiogram, CT or MRI may be necessary to detect liver, heart or kidney pathologies. U/S uses ultrasound signals where as CT uses x-ray and MRI uses the magnetic impulses to image an organ. Echocardiogram looks at the heart by using U/S technique. A study like U/S, CT or MRI may reveal an occult pus collection somewhere in the body that may have precipitated septic shock. Echocardiogram may identify a heart attack that was the culprit for shock.

Under special circumstances a biopsy study of an organ or tissue (for example kidney biopsy) may be necessary.

Management

The general managements of this life threatening condition include;

* Hospitalization of the patient
* Oxygen supplementation (mechanical ventilation if necessary)
* Swan-Ganz catheter may be necessary to assess hemo-dynamics

The specific management would depend upon the type of shock and it is usually approached along the lines as shown below.

Hypovolemic shock:

Rapid large volume intravenous fluid infusion with 14 to 16 gauze needle and about 2 liters of fluid is given in about ½ hour. 0.9% Normal saline or Ringer’s lactate are preferred.

Cardiogenic Shock:

Treatment of acute pulmonary edema if present (with diuretics, morphine, head propped up position, oxygen etc.

Hypotension is treated with drugs like nor-epinephrine, dopamine, dobutamine depending upon the degree of it & kidney status.

If acute heart attack is the cause then consider reperfusion therapy (primary coronary intervention or CABG or clot buster agents)

If compressive cardiogenic shock like cardiac temponade is present then immediate pericardiocentesis.
If tension pneumothorax is present immediate chest tube insertion and chest decompression.

Septic shock:

Rapid intravenous fluids about 2 liters in 1st ½ hour.
Antibiotics
Steroids
If disseminated intravascular coagulation with bleeding is present then fresh frozen plasma and platelet infusion.

Neurogenic shock:

Rapid intravenous fluids
Injection norepinephrine
Injection pheylephrine

Anaphylaxis/ Anaphylactic shock:

Injection epinephrine
Injection diphenhydramine or pheniramine maleate
Injection hydrocortisone

In addition to the above measures any precipitating or exacerbating causes for shock are identified and treated accordingly.

Pain is one of the most common manifestations of an underlying illness and its significance ranges from being only a discomfort to a signal of life threatening health conditions.

Pain is one of the features of a process called as inflammation which is the body reaction when it is injured or infected. In conditions like migraine headache pain serves no purpose to the body at all and just out-and-out annoying however sometimes it serves as the only clue to certain underlying pathologies like a cancer etc.

Peripheral mechanisms involved in pain mediation

The perception of pain occurs in the brain and it all starts when body encounters a pain producing stimulus like an injury such a stimulus will activate nerve fibers called as;

A delta &
C fibers.

The terminals of these nerve fibers are considered as receptors for the pain sensation, means the stimulation of these nerve endings will generate electrical signals and they are conducted across these nerve fibers and enter the spinal cord and eventually the brain where pain is perceived. These pain receptors are also called as primary afferent nociceptors or simply nociceptors.

The nociceptors also have a role in tissue protection and they do so by release of certain neuro-effector substances like substance P. This chemical released from the nociceptors facilitates several biological activities that primarily serve as a protective mechanism although as pointed above at time it is simply a nuisance and nothing else.

These pain receptors respond to several types of pain stimuli including;

* Heat
* Cold
* Irritating chemicals like bradykinin, serotonin, ATP, histamine
* Strong mechanical stimuli like pinching etc.

Central mechanisms involved in pain mediation

The following structures are involved;

* Spinal cord
* Spinothalamic tract (ascending pathway of pain)
* Thalamus
* Cerebral cortex

The nerve fibers from the peripheral pain receptors enter the posterior aspect of the spinal cord through peripheral nerves (e.g. sural nerve) and link themselves with the nerve cells called as neurons. They excite these neurons through certain chemical mediators like glutamate, substance P etc and the signals generated in the spinal cord neurons will travel upwards through the spinal cord then brainstem through the ascending pathway of pain named as spinothalamic tract.

The primary perception of pain for human beings occurs in the thalamus area of brain. But the exact localization, intensity & quality discrimination occurs in the parietal cortex of the cerebral hemispheres and thalao-cortical fibers connect thalamus with these areas of the cortex. From the thalamus fibers also project to other areas of cerebral cortex and they are related with the control of the emotional & behavioral aspects of the pain.

Certain special pain conditions

Referred pain:

This phenomenon is associated with pain originating from the visceral structures like heart, gall bladder, appendix etc. When there is some inflammation going on in these deeper structures the pain not necessarily will be experienced exactly in the skin overlying that particular structure rather it might be experienced else where, few examples include;

* Right shoulder pain with gall bladder injury
* Left shoulder pain with heart injuries
* Umbilical pain with appendix pain etc.

This phenomenon occurs due to what we call dermatomal distribution of sensory spinal roots. For example right sided c5 spinal root receives pain impulses from both gall bladder and right shoulder area. When gall bladder is inflamed because of same dermatomal distribution it might be referred in the shoulder area.

Sympathetically mediated pain syndrome:

There are mainly two types including;

* Causalgia &
* Reflex sympathetic dystrophy (RSD)

The above two conditions produce somewhat similar manifestations, causalgia occurs due to peripheral nerve injuries where as RSD occurs due to soft tissue injuries, fractures, stroke heart attack etc.

In the causalgia the injured peripheral nerve fibers acquire adrenergic sensitivity (autonomic sympathetic type) and mediate usually very uncomfortable & long duration pain even when the primary injury appears to have subsided. Swelling & discoloration of the limbs, thinning of bone (osteoporosis) and arthritic changes are frequently seen too. It is an example of sympathetic (adrenergic) over activity after an injury.

Neuropathic pain:

Although generally a damage to the peripheral or central pain pathways produce decreased or loss of pain sensation however paradoxically they may produce pain itself and this condition is called as neuropathic pain.

This type of pain may occur due to injuries to;

* Peripheral nerves
* Spinal nerve roots (pinched nerve root)
* Spinotalamic tract
* Thalamus etc.

Certain typical examples for above mentioned injuries include;

* Peripheral neuropathy
* Herpes zoster (shingles)
* Pinched nerve roots
* Thalamic stroke etc.

Neuropathic pain at times may be induced by even light touch and has very unusual tingling, burning or electrical-shock like quality. Patients generally have an area of loss sensation over the skin corresponding to the injured nervous pathway. They exhibit hyperpathia (minor painful stimulation is perceived as quite serve pain) & allodynia (non painful stimulation is perceived as pain).
Neuropathic pain is attributed to sensitization of the damaged area of the pain pathway to the stimuli. Normally such stimuli will not generate pain however due to the injury now these damaged site act as pain receptor that too in an exaggerated fashion.

Diagnosis

Pain is a subjective symptom and the presence of it should alert the physician of an underlying cause and accordingly a meticulous search must be done in this regard.

The investigations chosen depend upon what we are suspecting and examples include;

* Peripheral neuropathy;

Electromyography & nerve conduction studies
Blood tests
Nerve biopsy etc.

* Belly pain;

X-ray, ultrasound, CT or MRI of the belly
Blood tests (like liver function tests) etc.

* Headache;

CT or MRI of brain
CSF (cerebrospinal fluid) analysis
Angiogram of brain etc.

Chest pain;

Heart related (blood tests, ECG, Echocardiogram etc)
Lung related (e.g. chest x-ray, CT chest) etc.

Back pain;

CT or MRI of spine
Electromyography of the leg & back muscles etc.

Management

The management of pain will include the treatment for the pain itself as well as what caused it.

The treatment of the pain itself (symptomatic therapy) is accomplished by choosing drugs from the following groups;

NSAIDs (non steroidal anti-inflammatory drugs);

Paracetamol
Tramadol (also a narcotic drug)
Diclofenac
Piroxicam etc.

Opioids (narcotic);

Tramadol
Morphine
Pentazocin
Pethidine
Fentanyl skin patches etc.

Muscle Relaxants;

Tizanidine
Baclofen
Methocarbamol
Carisoprodol etc

Steroids;

Prednisolone
Dexamethasone
Methylprednisolone etc.

Anticonvlsants;

Gabapentin
Pregabalin
Sodium valproate
Carbamazepine etc.

Antidepressats;

Duloxetine
Amitriptyline etc.

Additional agents;

Ergotamine
Triptan medications
Drotaverine
Hyoscine etc.

The same medication or group of medications may not help with each & every condition. Below is a list of some of the commonly encountered pain conditions and in the bracket the commonly used medications for these conditions.

* Musculoskeletal pain (NSAIDs, muscle relaxants)
* Colicky (visceral) pain e.g. kidney stone pain (opioids, drotaverine, hyoscine etc)
* Cancer pain (long acting opioids like fentanyl skin patches)
* Acute migraine headache (ergotamine, triptan medications etc)
* Chronic migraine headache (amitriptyline, sodium valproate etc)
* Trigeminal neuralgia (carbamazepine, muscle relaxants etc)
* Back pain/pinched nerve root (e.g. gabapentin, muscle relaxants, NSAIDs, opioids) etc.

Edema is defined as an abnormal accumulation fluid in the interstitial tissue of the body and caused by varieties of disease conditions.

Tissue means a collection of similar cells that carry out certain functions in the body. Interstitial tissue lies between the cells of a structure and is predominantly made of fibrous tissue and abnormal amount o fluid may accumulate in it to produce edema.

Edema is a disease manifestation and its presence indicates the presence of an underlying disorder. A severe edema state is called as anasarca. The term edema is generally used for fluid collection in the interstitial area under the skin, and special forms of edema include ascitis (fluid accumulation in the belly cavity) & hydrothorax (fluid accumulation in the cavity around lungs produced by pleura).

What causes edema?

Around 60 to 70% of total body water is confined to the extra cellular space and about 70 to 75% of this water is present in the interstitial space and the remainder is in the plasma (the liquid part of blood devoid of blood cells).

The fluid in the interstitial & vascular compartments (inside the blood vessels) normally enjoys a balance in such a way that there is no excessive fluid accumulation in either of these compartments. The physiological forces that maintain this balance is governed by what is called as starling forces.

Thee forces are related with hydrostatic & colloid oncotic pressure of the vascular compartment with the oncotic pressure of the interstitial compartment and edema may generally result if one or more of factors are abnormal as below;

* Increased hydrostatic pressure inside the blood vessels
* Decreased oncotic pressure inside the blood vessels
* Increased oncotic pressure of the interstitial compartment

In addition to these three factors there are few more that contribute to the development of edema and include;

* Elevated permeability of blood vessel walls (occurs with inflammation)
* Impediment to the fluid clearance by the lymphatic system etc.
The following physiological systems assume a contributory role for the development of edema in diseased conditions.

* Renin angiotensin aldosterone (RAA) system
* AVP (arginine vasopressin)
* Endothelin etc.

Renin is a substance released in the kidneys and converts a protein substrate to angiotensin I. In the lungs angiotensin is converted in to angiotesin II and this substance in addition to its vasoconstrictor activity promotes secretion of a hormone from the adrenal glad by name aldosterone. This hormone acts on the kidney and facilitates the re-absorption of sodium. If rennin-angiotensin activity is excessive then it can cause abnormal sodium retention and can promote edema.

AVP (arginine vasopressin): This is a hormone secreted from the posterior pituitary gland and promotes re-absorption of free water from the renal tubules and collecting duct. The excessive action of this hormone can cause water retention and edema formation.

Endothelin: This substance is released from the endothelial cells and its level is elevated in heart failure patients and it causes narrowing of arteries to the kidneys, sodium retention and promotes edema.

Important causes of edema

* Congestive heart failure (CHF)
* Nephrotic syndrome
* Cirrhosis of the liver
* Severe malnutrition
* Hypo-albuminemia (due to any cause)
* Any condition favoring sodium & water retention
* Medication induced etc.

Let us find out now how some of these above listed conditions will promote the development of edema.

CHF: In CHF the pumping ability of the heart is compromised and this results in more blood pooling in the venous compartment. This will increase the pressure inside the venous side of capillaries and forces the fluid escape the vascular compartment into the interstitial compartment. The reduction in effective arterial blood volume will activate RAA system favoring sodium & water retention and further contributing to the edema generation.

Cirrhosis of liver: Cirrhosis promotes sodium retention by the kidneys; this and the decreased albumin levels will facilitate retention of fluid in the interstitial tissue. As with CHF the RAA system is activated and the end result is the same.

Hypo-albuminemic states: This condition causes decreased colloidal oncotic pressure and facilitates the development of edema. The clinical conditions associated with

* Nephrotic syndrome
* Severe malnutrition
* Severe chronic liver disease like cirrhosis
* Protein losing enteropathy etc.

Hypoalbuminemia, similar to above two conditions mentioned activates the RAA system with similar outcome.

Edema related with medication usage: There are different kinds of medications that can precipitate edema and they may do so by different mechanisms too.

Steroid preparations like prednisolone promote sodium re-absorption from the kidneys and causes sodium & water retention. Medications causing dilatation of arteries like hydralazine cause decreased effective arterial blood volume and activate RAA system. NSAIDs (non steroidal anti-inflammatory drugs) like indomethacin cause constriction of arteries of kidneys and activate RAA system. Drugs like interleukins cause edema by damaging the capillaries.

Clinical manifestations

Generally patients complain to the doctor about the swelling of legs or around the eyes or puffiness of face. Because of gravity effect the fluid in the day time may collect around the ankles in ambulatory patients and in bed ridden patients around the sacral area (lower back). If edema is not severe or in the early stages patients may not have noticed it so certain leading questions may be asked by the doctor to find out if patient has edema. For example if the patient has any difficulty in putting on or removing a ring from the finger, the shoes from the feet etc.

Diagnosis

Edema is a clinical diagnosis so the investigations that are ordered are mostly for identifying the cause of edema.

The investigations ordered in the setting of edema generally include;

* Blood tests
* Urine tests
* Imaging studies;

U/S (ultrasound)
Echocardiogram
X-rays
CT
MRI etc

* Special tests (ascitis, pleural fluid analysis etc)

Initial basic blood tests:

* Electrolytes like sodium, BUN, creatinine etc
* Serum albumin
* Liver function tests (LFT)
* Urine analysis (looking for albumin, creatinine etc)

The above routine blood tests will provide generally lot of initial clues as to the cause of edema. For example a low albumin level will lead towards causes like cirrhosis of liver. LFT may show findings suggestive liver dysfunction including cirrhosis. Urine analysis may show severe loss of albumin through the urine that may be suggestive of nephrotic syndrome.

Imaging studies including U/S, Echocardiogram, CT or MRI may be necessary to detect liver, heart or kidney pathologies. U/S uses ultrasound signals where as CT uses x-ray and MRI uses the magnetic impulses to image an organ. Echocardiogram looks at the heart by using U/S technique.

Management

The general measures of edema management include (on a case-to-case basis);

* Stabilizing the patient
* Hospitalization if necessary
* Fluid restriction
* Salt restriction
* High protein & nutritious diet
* Diuretics
* Taping of ascitis or hydrothorax if they are large (for symptomatic relief) etc.

Specific measures include the management of;

CHF – medications to augment the pumping action of the heart, ACE inhibitors, Beta blockers, CRT (cardiac resynchronization therapy) etc.

Nephrotic syndrome – steroids, immunosuppressive agents etc.

Malnutritional states – Protein rich nutritious diet etc.

Drug induced – If possible to switch over to other agents or reduce the dose etc.

Fever is an abnormally elevated body temperature and not a disease by itself rather it is a manifestation of certain underlying diseases.

The normal oral body temperature  for otherwise healthy individuals is around 98.2±0.7°F (36.8°±0.4°C) with generally the lowest temperature of the day is in the early morning (round 6 am) and the highest body temperature is around evening (around 4 pm). And these values represent most of the healthy individuals (about 98th percentile) and based on these facts;

“Fever can be defied as body temperature as measured by oral methods is >98.9°F (37.2°C) in the morning time or >99.9°F (37.7°C) in the evening time.

The core body temperature as measured by the rectal methods is supposed to be about 0.7°F (0.4°C) higher than oral method.

Distinction between fever & hyperthermia

It is difficult to touch the topic of fever without any reference to hyperthermia as there are certain similarities between them although there are differences too as noted below.

Elevated body temperature is either fever or hyperthermia. Before going to the finer details first let us familiarize with how fever & hyperthermia are produced?

A region in the brain called as hypothalamus regulates the body temperature. This region receives the inputs from two sources including;

* Temperature of the blood that bathes this region
* The peripheral nerves that conduct signals from the warmth/cold receptors in the skin

The above two types of signals are integrated in the temperature controlling areas of the hypothalamus so that optimum body temperature is maintained. Out of range body temperature either high (fever & hyperthermia) or low (hypothermia) all will have deleterious influence on the body functions and if severe can even result in death.

Coming back to the distinction between fever & hyperthermia; it is fever if it exceeds the normal daily variation and occurs together with an increase in the hypothalamic set point (e.g. 37°C to 39°C). On the other hand hyperthermia is characterized by an uncontrolled increase in body temperature that exceeds body’s ability to lose heat on the back ground of unchanged settings of hypothalamic thermoregulatory center. Also a fever may be mediated by pyrogens but hyperthermia does not involve such substances and it results from results from excessive;

* Heat production in the body or
* Heat exposure from the environment.

Types of hyperthermia include;

* Drug induced (cocaine, amphetamine etc)
* Heat stroke
* Serotonin syndrome (fluoxetine)
* NMS (neuroleptic malignant syndrome) – anti-psychotics like haloperidol
* Malignant hyperthermia (succinyl choline, inhalational anesthetics etc)
* Endocrine disorders (thyrotoxicosis etc)
* Central nervous system injuries – hypothalamic damage, stroke etc.

Diagnosis

The clinical diagnosis of fever & hyperthermia are accomplished by using a thermometer and checking the oral or core body temperature. Whenever possible a core body temperature should be measured as it is more reliable and less susceptible to external factors.

Once the diagnosis of fever is confirmed then a search will be done to look for its cause and if such cause is crystal clear then exhaustive investigations may not be always necessary. On the other hand if the cause is not clear then varieties of investigations are necessary. In general once a thorough history taking & examination is don majority of the time the physician will have some clue as to what may be the source of fever or hyperthermia

In general in the beginning one or few of these tests are all sufficient including;

* Blood tests (routine)
* Urine tests (routine)
* X-rays (chest, abdomen, bones etc)
* Blood cultures
* Urine cultures etc.

If the above tests either do not give any hints or give only partial hints then the following special tests may be necessary including;

* CSF (cerebrospinal fluid) analysis
* Aspirations of body fluids like pleural fluid
* Bone marrow biopsy
* Other tissue or organ biopsies etc.

In the blood tests routine CBC (complete blood count) may show increased WBC count. With bacterial infections generally neutrophils increase and with non bacterial infections like viral ones usually the lymphocytes increase although it is not a golden rule.

Urine analysis will be abnormal if UTI is present and shows findings like WBCs, increased protein, RBCs. Gram stain may show bacteria. Urine culture may grow the bacteria.

Chest x-ray is of immense value if lung pathology like pneumonia is suspected. I may also osteomyelitis (bone infection) etc. U/S, CT or MRI is not routinely necessary but if the preliminary tests do not help then they will be employed especially to look for occult pus collection etc. An echocardiogram may reveal endocarditis as a cause for fever.

If meningitis, encephalitis etc are suspected CSF analysis is mandatory.

Management

The management of fever & hyperthermia are dealt mainly at the following levels including the management of;

* The fever itself
* Its cause.

Fever specific treatments include;

* Stabilization of the patient
* Hospitalization if necessary
* Medications to reduce the temperature (paracetamol etc)
* Tepid sponging
* Adequate fluids (if required intravenous)
* Adequate nutrition etc.

The specific management

* Antibiotics for meningitis, UTI, pneumonia etc
* Aspiration or drainage of abscess (pus collections)
* Aspiration/drainage of pleural, peritoneal fluids
* Treat inflammatory conditions like lupus (steroids, immunosuppressive agents etc)
* Discontinue;

Drugs like haloperidol with NMS
Drug like SSRI in serotonin syndrome
Anesthetics, succniyl choline etc with malignant hyperpyrexia

However, body temperature varies from person to person, usually between 36-37 C. Your own temperature will also fluctuate throughout the day as it is affected by factors such as sleep, exercise, eating and drinking; and for women, the stage of the menstrual cycle that has been reached.

What causes high temperature?
Most fevers are caused by pyrogens fever-inducing toxins released by viruses or bacteria. Pyrogens act on the temperature regulating centre in the brain. Common illnesses caused by such infection are the common cold, tonsillitis, influenza and urinary tract infections cystitis. Fever may also occur in non-infectious conditions such as dehydration, heart attack or cancer.

In addition you can develop a high fever from over-exposure to heat, and especially to the sun. This is known as heat stroke.

In children, a high temperature may be caused by infections such as measles or an upper respiratory tract infection such as tonsillitis. For some children a high temperature can lead to convulsions or seizures which are caused by the effect that the fever has on the brain.

How is high temperature investigated and treated?
You can tell if you have a fever simply by taking your temperature with a thermometer. Placing one in the mouth will give you the most accurate reading.

To do this, put the bulb end of a clean thermometer under the tongue. Keep it there with the mouth closed for three minutes. On removal, check the temperature against the column of mercury.

Fever can be treated with antipyretic antifever drugs such as aspirin adults only, and paracetamol. These drugs also relieve any accompanying aches and pains. The underlying cause may also be treated for example with antibiotics, if it is due to a bacterial infection.

What can I do myself?
You can take an aspirin or paracetamal which in most cases will reduce your fever. Children can be given paracetamol at the first sign of fever. Repeat the dose every four to six hours as needed. Try to cool the body by stripping the person down and keeping them covered with a light cotton sheet, plus regular bathing in lukewarm water.

If heat stroke is causing the fever, move the sufferer to a cool shady place and remove as such clothing as possible. Place the person in a half sitting position and cover him or her with a wet sheet. Be sure to keep the sheet wet. Maintain a cool flow of air, ideally with an eletric fan, until the body temperature drops to 38 C. Then seek medical help immediately.

When should I see my doctor?
Do so if a fever lasts more than two days or if there are any other symptoms, such as severe headache with stiff neck, abdominal pain, or painful urination.

A very high fever is potentially dangerous as it can lead to coma in both adults and children. You should seek medical help immediately.

You should see the doctor if a fever occurs in a baby under six months old; in a child with a history of febrile convulsions seizures related to high temperatures; or in an elderly person.

SYMPTOMS
A fever may be accompanied by:
*Shivering
*Headache
*Sweating
*Thrist
*Flushed face
*Hot skin
*Rapid breathing

WARNING
Always see your doctor if your temperature remains above 38 C for longer than two days, or rinse obove 40 C. If you have taken aspirin or paracetamol and this does not reduce the fever, see a doctor as soon as possible.

In the case of babies, call your doctor if the temperature rises above 39 C, whatever the suspected cause. A high temperature can lead to seizures in some children.