Fluid/Temperature Regulation

this page:   Fluid retention -  NPE -  hypothermia -  hyperthermia
 

Fluid retention or oedema is the swelling that occurs due to fluid accumulating in the tissues, it may be localised to a certain body part or be generalised and affect the whole body. The most common symptoms are puffiness of the fingers, feet, ankles, legs and abdomen. In some cases urine may be passed infrequently or in small quantities. Symptoms Swelling and stiffness in the fingers, ankles and feet. Swollen breasts Frequent urination Shortness of breath Causes There are a number of causes of oedema ranging from simple, easily treated conditions through to serious and life-threatening diseases including kidney, heart and liver diseases, and cancer. It is important to consult your healthcare professional regarding your fluid retention in order to rule out these serious conditions before commencing self-treatment. Many mild cases are due to poor circulation such as occurs when sitting or standing for a long period, and fluid retention is a common symptom of varicose veins. Premenstrual syndrome is also a common cause, and is the likely diagnosis if your symptoms occur during the 10-14 days before your period starts, and are relieved afterwards. The weight gain and breast tenderness commonly experienced in premenstrual syndrome are largely caused by fluid retention. People with arthritis often find that they experience fluid retention around the affected joints in addition to the pain, stiffness and other characteristic arthritis symptoms. Oedema can also be caused by an excess of salt in the diet, as a side-effect of certain medications, and by the surgical removal of lymph glands. If you suspect your medication is responsible for your fluid retention discuss your concerns with your healthcare professional, who may prescribe a diuretic medication (a medicine which stimulates urination and thereby relieves the fluid retention). Natural Therapies Vitamin B6 is essential for the hormone which triggers the body to urinate; it is commonly deficient during pre-menstrual syndrome and may help to relieve fluid retention at this time Herbal diuretic medicines which may be of assistance for the relief of fluid retention include dandelion leaf, horsetail and corn silk Celery seed and juniper berries are herbal diuretics with special application to arthritic Conditions Lifestyle Factors Even though it may seem likely to worsen the situation, it is important to maintain a normal intake of water, 6 to 8 glasses per day, when you have fluid retention. This will help to flush the fluid through the kidneys and avoid the build-up of toxic wastes. Dietary intake of salt should be restricted if you suffer from fluid retention, as it causes the body to retain water. At first you may find that food is not as tasty as you are used to, but over a few weeks your taste buds will become accustomed to the reduced saltiness, and you will find yourself noticing different tastes in your food. If troubled by mild oedema, adopt a healthy eating plan and gentle exercise program along with a herbal diuretic, to help you achieve or maintain your ideal bodyweight and reduce accumulated fluids. Prevention Avoid crossing the legs, standing for long periods of time and wearing tight clothing as these may all restrict circulation. It may also be helpful to lie with your legs elevated against a wall at the end of the day, or to raise the foot of your bed a few centimetres off the ground. This allows gravity to assist the circulation and fluid to flow back up the legs. Maintain a healthy diet rich in fruits and vegetables and low in salt. Try to include two litres of water in your diet every day. Important Things Many causes of fluid retention are simple and easy to treat, but others may be very serious. Always consult your health care professional before commencing self-treatment, and particularly if you are taking medication for high blood pressure or other cardiovascular conditions.

NPE many of us with forms of MSA just expire after a seemingly innocent infection. FOR US THERE ARE NO INNOCENT MINOR INFECTIONS.  Now I'm going to take a diuretic (thiazide), some pseudo-ephedrine and kick back a bit more, if I ease up and take care it should pass as it always has -- somehow I never remember one time to another LOL --------------------------------------------------------------------------------  Pulmonary Edema, Neurogenic  Authored by Sat Sharma, M.D., Program Director, Assistant Professor, Sections of Pulmonary Medicine & Critical Care Medicine, University of Manitoba, Winnipeg, Canada . Sat Sharma, M.D. is a member of the following medical societies: American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Sleep Disorders Association, and American Thoracic Society INTRODUCTION   Background: Neurogenic Pulmonary Edema (NPE), a relatively rare form of pulmonary edema represents an increase in pulmonary interstitial and alveolar fluid, developing within few hours of a well defined neurologic insult. Pathophysiology: The pathogenesis of neurogenic pulmonary edema remains incompeletely understood. Since the most common neurologic events are associated with increased intracranial pressure, intracranial hypertension is considered to be a key etiologic factor. The sites wthin the central nervous system which are critical to the development of NPE are not fully established. Potential roles for the hypothalamus, the medulla, elevated intracranial pressure, and activation of sympathetic system is suggested based on animal experimentation. NEUROANATOMIC STRUCTURES:   ·The medulla oblongata is believed to activate sympathetic component of the autonomic nervous system. Experimentally, bilateral lesions of the nuclei in medulla produce profound pulmonary and systematic hypertension as well as pulmonary edema. ·Alpha adrenergic blockade (with phentolamine) and spinal cord transection at C7 level is able to abolish the formation of NPE, suggesting important role for sympathetic activation. ·Possibly, acute neurologic crisis accompanied by marked increase in intracranial pressure, stimulates the hypothalamus and the vasomotor centres of the medulla. This in turn initiates a massive autonomic discharge mediated by preganglionic centres within crevical spine.   MECHANISM OF EDEMA FORMATION:   A central nervous system event produces a dramatic change in Starling's forces which govern movement of fluid between capillaries and the interstium and/or increased pulmonary capillary permeability. Changes in capillary hydrostatic pressure:   Alterations in pulmonary vascular pressures appear to be the most likely Starling's force to influence the formation of NPE. Experimental observations have suggested following mechanisms by which pulmonary capillary hydrostatic pressures could be acutely increased: An increase in left atrial pressure may occur due to increased sympathetic tone and increase in venous return. Left ventricular performance may deteriorate secondary to the direct effects of catecholamines and other mediators as well as transient systemic hypertension. Pulmonary venoconstriction is known to occur with sympathetic stimulation, which may increase the capillary hydrostatic pressure and produce pulmonary edema without affecting left atrial or pulmonary capillary wedge pressure. Changes in pulmonary capillary permeability:   An increase in capillary permeability could result in NPE without the elevation of pulmonary capillary hydrostatic pressure, as cuasative hemodynamic alteration is inconsistent. However, the evidence is that alpha adrenergic blockade can protect against NPE, therefore epinephrine or norepinephrine or even release of secondary mediators may directly increase pulmonary vascular permeability. An initial rapid rise in pulmonary vascular pressure due to pulmonary vasoconstriction and or pulmonary blood flow could lead to pulmonary microvascular injury. Consequently there occurs an increase in vascular permeability and edema formation, as suggested by frequent observation of pulmonary hemorrhage (Blast theory). Frequency:  In the U.S.: Upto a one-third of patients with status epileptics have evidence of NPE. Over one half of patients with severe blunt or penetrating head injury are associated with NPE. Seventy one percent of the fatal cases of subrachnoid hemorrhage were complicated by NPE. NPE may complicate subarachnoid and intrcerebral hemorrhage in 30% to 70% of patients and may recur after initial resolution.  Mortality/Morbidity: Outcome is usually determined by the course of neurological insult which produced neurogenic pulmonary edema. CLINICAL History: NPE characteristically presents within minutes to hours of a severe central nervous system insult. Sudden onset of dyspnea is the most common symptom, and mild hemoptysis may occur in many patients. Physical: The physical examination generally reveals tachypnea, tachycardia, bibasilar crackles, and respiratory distress. Findings of pulmonary edema are present with normal jugular venous pressure and absence of cardiac gallop. Causes: The etiologies of NPE are listed below: Major causes:  Epileptic seizures  Cerebral hemorrhage  Head injury  Minor Causes:  Multiple Sclerosis with medullary involvement  Nonhemorrhagic strokes  Bulbar poliomyelitis  Air embolism  Brain tumours  Electroconvulsive therapy  Bacterial meningitis  Cervical spinal cord injury  DIFFERENTIALS Adult Respiratory Distress Syndrome (ARDS)  Aspiration Pneumonia    Other Problems to be Considered:    Aspiration pneumonia also occurs in the settings of altered conciousness. NPE tends to develop more rapidly than aspiration pneumonia and is not associated with fever. Aspiration pneumonia may take 1 to 2 weeks to resolve whereas NPE resolves within hours to several days. Congestive heart failure WORKUP Lab Studies:  Not helpful in making a diagnosis.  Imaging Studies:  ·CXR radiograph shows a normal size heart with bilateral alveolar filling process.  ·CXR may mimic congestive heart failure with cephalization of blood flow although other features of heart failure such as septal lines are usually not evident.  Procedures:  · Hemodynamic measurements with a Swan-Ganz catheterization may be necessary to differentiate NPE from hydrostatic or cardiogenic pulmonary edema. Blood pressure, cardiac output and pulmonary capillary wedge pressure are usually normal by the time NPE is diagnosed.  TREATMENT Medical Care:  The outcome of patients with neurogenic pulmonary edema is determined by the course of the neurological insult, the treatment should focus upon the underlying disorder. NPE is generally managed in a supportive and conservative fashion, the majority resolve within 48 to 72 hurs. General Supportive care:  ·Supplemental oxygen is usually required.  ·Mechanical ventilation either non-invasive with a face mask or via endotracheal tube may be necessary in some patients.  ·High levels of positive end expiratory pressures (PEEP) may be required to treat severe hypoxemia, but caution is advised because it can inhibit cerebral venous return and worsen the intracranial hypertension.  ·Maintenance of low cardiac filling pressures may decrease edema formation but adequate cardiac output and the cerebral perfusion pressures should be maintained. Swan-Ganz cathetrization may be helpful in guiding fluid and hemodynamic management.  Alpha adrenergic antagonists:  Alpha adrengeric blockers (eg, phentolamine) can prevent or hasten the resolution of NPE in experimental models. No human trials have established the safety and efficacy of these agents.  These agents may be used to treat concomitant systematic hypertension if present, but significant hypotension that can diminish cerebral perfusion must be avoided.  Other agents such as beta adrenergic blockers, dobutamine and chlorpromazine have been advocated but assessment of their effectiveness is difficult because NPE is usually a self limited condition.  FOLLOW-UP Further Inpatient Care:  These patients are usually admitted to the hospital, intensive care admission may be rquired if the patient develops worsening hypoxemia or respiratory distress.  Prognosis:  Most of the times NPE is rather well tolerated and the disease resolves within 48 to 72 hours. The prognosis is determined by the course of underlying neurological problem.   top of page

hypothermia Temperature disorders Marla Gendelman MD Mechanisms of heat loss Core temperature is determined by the balance of heat loss/gain. In the operating room, heat loss is more common than heat gain. Special efforts should be made to avoid heat loss, due to the consequent changes in the various organs systems that can occur. These changes can result in morbidity in the postoperative period as described below. Radiation: energy transfer via electromagnetic waves, no direct contact needed. Radiant losses can be responsible for up to 50% of heat loss in the OR and is proportional to the 4th power of the radius. Convection: heat transfer by air movement and depends on air velocity, temperature and exposed surface area. Evaporation: occurs primarily through perspiration, but can occur from the respiratory tract and open body cavities. Evaporation is the main mechanism by which the body prevents hyperthermia in a warm environment. Evaporation can exchange heat against a thermal gradient. Evaporation accounts for 25% of heat losses. Conduction: is the transfer of heat by direct contact with a stable medium (cool prep or irrigating solution, cold OR table) and accounts for 10% of heat losses in OR. Mechanisms of Heat Gain   Basal metabolism: accounts for all the net heat production in a neutral thermal environment. At rest, major organs supply 50-60% of body heat and muscle movement supplies 20%. Voluntary movement: exercise can increase heat production up to 90%, this is not possible under anesthesia. Shivering can increase heat production as much as 400-500%. Shivering is not effective over the long term because of fatigue. Shivering ceases at body temperatures under 33°C . Shivering can cause: Increased O2 consumption, increased CO2 production, increased ventilatory demand, increased myocardial work, decreased arterial O2 saturation Nonshivering thermogenesis: can be an effective method of thermogenesis and is most common in neonates. It occurs primarily through the metabolism of brown fat and is mediated by noreprhephrine. Brown fat stores in a neonate are located in the body's core and are highly vascular. Control of Body Temperature   Peripheral cutaneous thermoreceptors relay temperature information to the lateral spinothalamic tract to the anterior hypothalamus. The anterior hypothalamus also contains central receptors which respond to the temperature of the blood. Together, the anterior and posterior hypothalamus establish a reference temperature or set point. This set point is affected by age, exercise, medications, anesthetics and other factors. When a difference is detected between the set point and the actual body temperature, the appropriate heat preservating or heat generating response is initiated by the posterior hypothalamus. The core or central sensors are more dominant and exert a more overriding control over the peripheral receptors. In addition to the posterior hypothalamus initiating heat conserving or heat generating responses, the cerebral cortex coordinates behavior responses. Measuring Body Temperature Measuring core temperature is important in the perioperative period and not all sites of measurement are created equal. Esophageal temperature: measured at the level of the heart, is the closest to mixed venous blood tempe rature and is considered to be the best measurement of core temperature. However, limitations exist to this method of measurement and include probe placement in the lower one third of the esophagus. Incorrectly placed probes measure inaccurately. Additionally, an open chest for a cardiac or thoracic procedure will make temperature measurement by this method inaccurate. Nasopharyngeal temperature:: a temperature probe in the nasopharynx positioned posterior to the soft palate, provides an estimate of hypothalamic temperature. This method is inaccurate with an uncuffed endotracheal tube and can cause trauma to the nasopharynx. Tympanic Membrane: Temperature: tympanic membrane temperature probes closely approximates hypothalamic temperature, but are limited by cerumen in the ear canal and probe placement. Trauma to the ear canal or tympanic membrane can occur. This method is a highly reliable method of measurement of core temperatures. Bladder Temperature:: measurement of bladder temperature compares favorably to temperature measured with rectal, nasopharyngeal and esophageal probes. There are obvious inaccuracies during abdominal or urologic procedures. During cardiopulmonary bypass procedures, bladder temperature has been found to be an accurate method of temperature measurement. Rectal Temperature:: rectal temperature is usually a few tenths of a degree higher than arterial blood temperature. This method of measurement can be affected by cool blood returning from the lower extremities, insulation by feces and heat producing bowel organisms. Oral Temperature: oral temperature poorly reflects core temperature and tends to be 0.3-0.65o C below rectal temperature. Oral temperatures are used for convenience, but may be clinically misleading. Axillary Temperature:: the axilla is convenient to measure temperatures, but is very inaccurate. It is generally 0.5oC below oral temperatures and 1oC below rectal temperatures. It is a poor measurement of core temperature, but can be used to measure general temperature trends. Skin Temperature: Skin temperature measurement by liquid crystal discs or strips has several shortcomings, the most important being accuracy. Etiology of Hypothermia Hypothermia can be divided into three stages.- 36-32 C, moderate - 32-30 C and severe - <30 C. Hypothermia is a very common perioperative problem. Conditions that contribute to hypothermia Pre-existing medical conditions may impair thermoregulation and include:   Hypothyroidism, hypoadrenalism, circulatory failure, peripheral nervous system disorders and malnutrition. Administration of preoperative medications such as narcotics, sedatives and hypnotics may impair temperature regulation. Lack of clothing and cold rooms and hallways also contribute to reductions in body temperatures. Extremes of decreased muscle mass can contribute to cold intolerance. Operating room conditions such as low ambient temperature and humidity in the OR contribute to the loss of body heat. Laminar airflow systems can also increase convective heat losses. Anesthetics can interfere with thermoregulation in several ways: Cold unhumidified gases delivered via an endotracheal tube directly to the lungs bypass he heating and humidifying system of the nose and nasopharynx. Volatile anesthetics cause vasodilation and further increase radiative and conductive heat losses. Muscle relaxants abolish shivering and the body loses one of it's methods to generate heat. Epidural and spinal anesthesia has been demonstrated to produce even greater heat losses than general anesthesia because of the vasodilation from the sympathetic blockade. Other factors that contribute to perioperative heat loss include administrative of fluids, cold irrigating fluids or cold blood. Physiologic Consequences of Hypothermia The physiologic consequences of hypothermia usually become apparent postoperatively. The major concerns in the postoperative period include shivering, peripheral vasoconstriction and delayed drug clearance.  Shivering can produce an increase in metabolic rate up to 500%. This causes increased oxygen consumption and greater carbon dioxide production which can increase ventilatory requirements. Myocardial oxygen consumption increases because of increased cardiac output and myocardial work. Myocardial ischemia can occur particularly in patients who are elderly or have pre-existing coronary artery disease.  Peripheral vasoconstriction can cause hypertension and increased systemic vascular resistance. This can increase myocardial work and increase myocardial ischemia. Vasoconstriction can mask hypovolemia causing hypotension as the patient warms and vasodilates.  Delayed drug clearance is more significant in elderly patients and other patients who may already have impaired drug clearance mechanisms. The maximum renal clearance of a drug can decrease 10% for every 0.6oC fall in temperature. This can delay the clearance of muscle relaxants.  Other Physiologic Consequences of Hypothermia  Cardiovascular Myocardial depression,Ventricular arrhythmias, increased blood viscosiy, decreased effective blood volume, increased pulmonary and systemic vascular resistance.  Neurologic Decreased cerebral blood volume, Impaired mentation, hypothalamic dysfunction.  Renal Decreased renal perfusion, decreased tubular reabsorption (cold diuresis), acute tubular necrosis.  Gastrointestinal Decrease intestinal motility/ileus,increase susceptibility to ulcers.  Metabolic Increased oxygen consumption, metabolic acidosis, decreased insulin production, electrolyte imbalance, altered hepatic clearance. Pulmonary Decreased alveolar ventilation, pulmonary edema,increased dead space ventilation.  Prevention of Hypothermia   A number of measures can be undertaken to minimize heat loss in the operating room. Ideally, preventive measures should be undertaken at the start of a case since the majority of heat loss occurs within the first hour. Raising ambient room temperature is an effective method. A critical temperature of 21oC exists for adults below which most patients will become hypothermic. Room temperature should ideally be maintained until the patient is prepped and draped. Humidification of inspired gases to 37oC and 100% relative humidity effectively maintains normothermia and can warm hypothermic patients. Humidification alone can reduce hourly heat loss up to 15%. Expired gas temperatures >43oC can cause airway burns. Blood and fluid warmers can be used. Infusion of 600 cc of cold blood or fluids can lower core temperature 0.5oC. Rapid infusion of 10 .... of cold blood has been documented to cause cardiac arrest due to hypothermia. Warmed blood has decreased viscosity and can induce vasodilation. Warming fluids alone is not an effective method to reverse hypothermia. Low flow rates and long tubing can allow the temperature of the fluid to cool before reaching the patient. Warming blankets can reduce convective heat losses to the cold table, particularly in pediatric patients. Risks include burns, especially if prop solution is allowed to pool under the patient. Reflective blankets may or may not help in the setting of hypothermia, although the risks are minimal. Postoperative Care   At core temperatures below 33oC, or even higher in elderly patient or patients with underlying medical conditions, reduced cardiac output, arrhythmias and CNS impairment are likely. These patients should not be extubated prior to rewarming. Core rewarming techniques may be implemented if necessary.  top of page

Hyperthermia Etiologies of Hyperthermia   Hyperthermia is less common than hypothermia and becomes clinically significant at core temperatures exceeding 40oC. Postoperative fever must be distinguished from other hyperthermic syndromes. Fever results from a resetting of the normal set point temperature, whereas other hyperthermic states temperature rises despite the body's heat dissipating mechanisms. During fever until the new set point is reached, heat generating mechanisms such as shivering and vasoconstriction are activated. Unlike hyperthermia, fever activates no physiologic mechanisms such as vasodilation and sweating to bring the temperature down. Common causes of hyperthermia   Blood transfusion, Warm environment,Drug induced fever Infection Endocrine disorders Anticholinergics Hypothalamic injury Malignant hyperthermia Neurogenic hyperthermia Neuroleptic malignant syndrome over use of heat conservation methods. Neurogenic Hyperthermia   Neurogenic hyperthermia occurs when lesions exist in the contramedial forebrain near the third ventricle. Trauma, emboli, tumor and intracranial manipulation have been observed to cause this condition. Prostaglandins are theorized to act on the anterior hypothalamus to cause the fever. Most treatment is ineffective although indomethacin may be of some help. Fever   Fever is a resetting of the body's temperature to a higher level. The patient seeks heat, vasoconstricts and has a reduction in sweating. Metabolic rate rises. Fever can be beneficial in the body defense against infection. Leukocyte function and antibody production is enhanced. Virus reproduction may be interrupted by fever. Fever is mounted in a response to circulating pyrogens released by leukocytes. Pyrogens induce the release of prostaglandin E1 and E2, which act on the neurons of the preoptic area of the hypothalamus. This process causes core body temperature to set higher. Causes of Postoperative Fever The causes are varied but the most common are: Heat gain in the surgical environment  Transfusion reaction (leukocyte reaction)  Sepsis  Atelectasis/aspiration (rare in the first 24 hours post-op)  Dehydration (particularly in pediatric patients)  CNS damage  Fat emboli  Drug reaction  Phlebitis/deep vein thrombosis  Pulmonary emboli  Malignancy Treatment of Hyperthermia Cooling by evaporative methods (cool room, wet skin)  Cooling by direct external methods (pack in ice)  Gastric or peritoneal lavage with iced saline  Cardiopulmonary bypass or hemodialysis (monitor closely for cardiovascular instability). Treatment of Fever Note: attempts to cool a febrile patient may be overcome by the patient's thermoregulatory system Use antipyretics (prevent prostaglandin synthesis  Sponge bath with tepid water  Cool environment  Evaporative measures (cover patient with wet sheet, cool room)  Hypothermia blanket  Monitor fluids and electrolytes closely  top of page

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last update 03/2005

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