General Systemic States (Animal Internal Medicine) PDF

GENERAL SYSTEMIC STATES By Dr. Asmaa G. Saleh lecturer of Animal internal medicine Faculty of Veterinary Medicine Damanhur University  Definition There are several systemic alterations which contribute to the effects of many...

GENERAL SYSTEMIC STATES By Dr. Asmaa G. Saleh lecturer of Animal internal medicine Faculty of Veterinary Medicine Damanhur University  Definition There are several systemic alterations which contribute to the effects of many disease. I. Variation of body temperature 1.The body temperature is a reflection of the balance between heat gain and heat loss. a. Heat gain: produced by muscular, metabolic activities and absorption from environment (radiation, conduction, convection). absorption or emission a transfer of of electromagnetic transfer of heat heat between two radiation at the body between media at different surface, and depends two media that are in temperatures, such on the skin surface direct contact, such as as the coat surface temperature and area. the skin and water. and the air. b. Heat loss: through sweating, profuse salivation, respiration, during defecation and urination. The balance between heat gain & heat loss is controlled by Peripheral Heat regulating function of Thermo-receptors in the Hypothalamus skin Maintain relative constant body T. Homeothermy  A. HYPOTHERMIA Subnormal temperature Due to Insufficient Excess and/or heat heat lost production  Excess heat lost Due to exposure to severe cold air and the metabolic activity, muscular tone and peripheral vasoconstriction are unable to compensate  Insufficient heat production 1. Decrease of muscle tone as in parturient paresis and acute ruminal impaction. 2. During anesthesia & sedation. 3. Decreased tissue perfusion(peripheral vasodilatation) in shock. 4. Anemia & severe hemorrhage. 5. Terminal stage of many diseases due to reduction of metabolic activity. 6. Very old & badly nourished animals. 7. (pre-mortal fall) Shortly before death in a previously feverish animal (except in strychnine poisoning, tetanus, heat stroke). 8.Acute enteritis with sever diarrhea.  Clinical findings 1. Weakness & general depression. 2. Low body temperature. 3. Decrease respiratory rates. 4. Cool & dry of oral mucous membranes. 5. Coldness of the skin & extremities. 6. Complete anorexia. 7. Bradycardia, weak arterial pulse & collapse of major veins.  NEONATAL HYPOTHERMIA  Neonates can't maintain their body temperature at normal value after birth under cold environmental condition.  A major cause of morbidity & mortality in newborn farm animals within the first few days of life. Especially kids & lambs  Factors that increase the susceptibility of neonate to hypothermia  Poor condition of pregnant dam.  Young or old dam.  Multiple births.  Dystocia.  Neonate with low birth weight or born prematurely.  Wetting of birth coat or exposure to wind.  Clinical signs Early stage of hypothermia  Shivering & trembling.  Skin of the extremities & ears feels cool to touch.  Within hours after birth: B. temperature in neonatal calves, lambs, kids, foals which exposed to a cold may reach to 35°C or following 12-24 hrs of profuse diarrhea accompanied by marked dehydration & acidosis.  A weak suck reflex.  Sternal recumbence.  Late stage of hypothermia  Heart rate is slower than normal.  The intensity of the heart sounds is decreased.  Further weakness.  Coma.  Death in a few hours.  Clinical pathology In neonatal calves & lambs with hypothermia..Serum glucose Reduced Non-esterified fatty acids (NEFA).immunoglobulins Hemoconcentration..Azotemia Metabolic acidosis.  Treatment 1. Treatment of the primary causes. 2. Complete rest in good ventilated warm place. 3. I.V. inj. of glucose, Ca, Mg to increase muscle tone. 4. Lambs < 5 hrs of age with severe hypothermia (< 37°C) are dried off and given intra peritoneal injection of 20% glucose at a temp. of 39°C: at dose: 50 ml for a large lamb (>4.5 kg). 35 ml for a medium lamb (3.0-4.5 kg). 25 ml for a small lamb (3.0 kg). 5. Colostrum or milk should be warmed to 40°C & intubated using an esophageal feeder. Esophageal feeder.  Control 1. The sick & neonate animal should be housed in an environment with minimal drafts. Good housing of diseased foal & calf. 2. Excessive moisture should be removed from animal's coat. 3. Insulation with rugs & leg bandages especially in foals. 4. Energy intake should be sufficient. 5. Frequent monitoring of both rectal and air temperature. Horse protected by rug. Foal protected by leg bandages.  B. HYPERTHERMIA (HEAT STROKE or HEAT EXHAUSTION) Elevation of body temperature due to Excessive Deficient heat lost heat production When the causes are purely physical  Etiology 1. Physical major causes High environmental temperature &Prolonged sever muscular exertion specially ( in high humidity, fat animal with heavy coat, inadequate ventilation). 2. Neurogenic hyperthermia by damage to hypothalamus. 3. Dehydration due to insufficient tissue fluids to accommodate heat loss by evaporation. 4. Excessive muscular activity as in strychnine poisoning. 5. Excessive administration of some drugs e.g. Levamisole (para sympathomimitic), calcium.  Pathogenesis I. Unless the body temp. reaches a critical point 1- Short period of hyperthermia is advantageous in infectious disease  Facilitate phagocytosis  Stimulate immune bodies production  Impaired viability of m.os. 2- The metabolic rate increased by 40-50% leading to - Hypoglycemia. - Depletion of liver glycogen. - Increased catabolism of protein. 3- Anorexia due to dehydration. 4-Increased thirst due to dryness of mouth. 5- Increased heart rate due to ↑ blood temperature - Peripheral vasodilatation→ ↓blood pressure 6- Respiration increased in rate and depth due to the effect on respiratory center). 7- Peripheral vasodilatation → ↓renal blood flow → decreased urine secretion (oliguria).  II. Body temperature exceed a critical point. Circulatory Depression of Heart rate failure nervous fast & irregular. due to & myocardial respiratory weakness. center causes Death by respiratory failure  Clinical findings Rise in body temperature >39.5C (103F) death occurs in degree >42.5C (108F). 1. In the early stages, there is increase thirst, the animal seeks cool places & often lying in water. Hyperthermia in dogs. 2. Sweating and salivation occur initially, followed by a marked absence of sweating. Hyperthermia, sweating and salivation in dog and cows. 3. The animal may restless, dull, stumbles, while walking and tends to lie down. Calf with hyperthermia, restless and dull. 4. Abortion may occur if the period of hyperthermia is prolonged. 5. When the body temperature reaches 41.5-42.5C  Respiration is labored then become shallow & irregular.  Heart rates are increased. The pulse becomes very rapid & weak followed by collapse, convulsions, coma then death.  Clinical Pathology 1. No important clinic-pathological change in simple hyperthermia. 2. Hyponatremic dehydration and azotemia in horses with advanced hyperthermia.  Necropsy findings. 1- Peripheral vasodilatation. 2- Rigor mortis occur rapidly. 3- Poor, slow, incomplete clotting of blood.  Measure taken to manage heat stress: 1. Provide cool clean water for drinking. 2. Use shades and intermittent sprinkler system. 3. Enhance air-flow by fans. Manage heat stress.  4. Rations & feeding of animals in the evening. 5. Minimize handling during periods of greatest heat stress. 6. In exercising horses, periodic rests in the shade with fans & water sprinklers. 7. Sheep are protected by shedding of the wool. Manage heat stress.  Treatment 1. Complete rest in cold and good ventilated place. 2. Injection of saline 0.9 % & dextrose 5% i.v. contains analgesic and antihistaminic drugs. Horses often need 20-40 liters of fluids over the first few hours of treatment. Fluids can also be administered orally, but care should be taken to ensure that gastrointestinal motility is not impaired. 3. Cold fomentation by water or ice bag on the extremities. 4. Cold enema with analgesic. 5. Tranquillizer is recommended to reduce unnecessary activity. N.B. Calcium preparation is contraindicated in hyperthermia. Immersion in ice baths or cold water is absolutely contraindicated because this practice causes peripheral vasoconstriction. Vasoconstriction results in further elevation of core body temperature.  C. FEVER (Pyrexia)  An elevation of body temperature above that normally maintained by animal.  It is a combination of hyperthermia & infection or inflammation  Combination of hyperthermia and toxemia produced by substances circulating in the blood stream.  Etiology Septic fever (common) Aseptic fever Infection with bacteria, viruses, 1. Chemical fever caused by protozoa, fungi inj. of foreign protein. 2. Surgical fever due to 1. Localized infection such as breakdown of tissues & abscess, cellulitis, empyema blood vessels. 3. Fever from tissues necrosis 2. Generalized infection (i/m injection of necrotizing material) as in bacteremia & 4. Severe intravascular endocarditis (intermittent) hemolysis & extensive infarction. 3. Generalized infection as in 5. Immune reactions, septicemic diseases, viremia, anaphylaxis & toxemia (Consistent) angioneurotic edema. 6.Extensive necrosis in rapidly growing neoplasm  Pathogenesis Exogenous pyrogens (bactaria,virus, bact. Endotoxin, Ag-Ab complex, Hb) ↓ Phagocytes (macrophges, monocytes) ↓ Interleukin-1(endogenous pyrogen) ↓ Hypothalamus(anterior) ↓ Abrupt ↑ in synthesis of PGE2 ↓ Raise thermostatic set point of hypothalmus ↓ Mechanisms of heat conservation(vasoconstriction) and production(shivering thermogenesis) to ↑ blood temperature until match the hypothalamic set point.  Stages and clinical signs of fever 1. Increment Cutaneous vasoconstriction resulting coldness and “chill” dryness of the skin (cold extremities) & absence of sweet. muscular shivering Reduced respiratory rates Increased pulse rates & rectal temp. Reduced urine formation. 2. Fastigium Cutaneous vasodilatation causes flushing of the skin “constant and mucosa. temperature” Severe sweating and diuresis. Decrease ruminal motility & constipation. 3. Decrement Excess stored heat is dissipated. “fever defervescence” Vasodilatation, sweating & muscle flaccidity. Falls in degree of body temperature.  The increased body temperature Increases leukocyte motility, bactericidal and phagocytic activities. Increase lymphocyte transformation. Enhances the effects of interferon and interleukin-1.  Adverse effects of fever Anorexia, wasting (excessive catabolism if prolonged).  Effects on the CNS lead to convulsions. Hyper pnea, Increase in heart rate. increased thirst & scant feces. Oliguria & albuminuria. Depression & muscular weakness. The temperature elevation is rarely above 42°C (107°F). If the toxemia accompanying the hyperthermia is sever, continuous the ability of tissues to respond to heat production or conservation may be lost and as death approaches, there is fall in body temperature (heat collapse).  Treatment ▪ Control of infection and remove source of infection by antibacterial drugs. Depending on the cause of the disease, in fever of unknown origin use broad spectrum antibiotic. ▪ If the fever is high enough or prolonged to cause discomfort , anorexia or death use antipyretics (Analgin, novlgin, ….. ▪ Antidote for toxins. ▪ Cold fomentation by cold water or ice bag or fomentation with alcohol or vinegar. ▪ Fluid therapy (5% dextrose or saline solution). ▪ Glucocorticoids to facilitate repair and alleviate inflammation accompany infection - Antihistaminic.