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Parenteral nutrition was instituted in a malnourished woman with a low serum phosphorus. In spite of a moderate phosphorus intake, the serum phosphorus descended to very low levels before returning to a normal range. Over a three week period she was troubled by paraesthesias, numbness, and a generalised weakness. The cause was thought to be hypophosphataemia.
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PMID:Hypophosphataemia and paraesthesias during parenteral nutrition. 82 75

Severe hypophosphatemia (i.e., serum phosphorus concentration below 1 mg/dl) occurs infrequently in veterinary patients. It is most often associated with diabetic ketoacidosis in small animals. Phosphate is necessary for the production of 2,3 diphosphoglycerate (2,3-DPG) and adenosine triphosphate (ATP); both are important for normal cellular metabolism. Consequences of severe hypophosphatemia may include hemolytic anemia, seizures, altered mentation, cardiomyopathy, and skeletal muscle weakness. Parenteral phosphate therapy is necessary in most cases of severe hypophosphatemia.
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PMID:Hypophosphatemia. Causes and clinical consequences. 267 24

A 42-year-old man suffered from erythema chronicum migrans on different parts of the body after repeated tick bites. A few months after the last tick bite he developed a painful neuropathy in both legs with patchy disturbance of sensibility, mild weakness of the feet and loss of the right ankle jerk. Repeated determinations of antibodies against borrelia spirochetes revealed increasing IgG titres. Biopsy of the left sural nerve, which was clinically and electrophysiologically affected, showed a vasculitis of epineurial vasa nervorum and severe angiopathic lesions of the perineurium and the neural parenchyma. Parenteral high-dose penicillin treatment resolved the clinical symptoms.
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PMID:Neuropathy of vasculitic origin in a case of Garin-Boujadoux-Bannwarth syndrome with positive borrelia antibody response. 300 23

Adequate nutrition in the severely burned child often determines the morbidity and mortality and its supervision demands a high priority in the management of the burn injury. A disciplined, detailed programme is required, but this is often neglected. The hypermetabolism experienced in the severe burn may require a calorie intake up to 2 1/2 times normal, and in the growing child, with extra requirements, a negative balance can easily eventuate if careful management is not instituted. A daily metabolic plan provides firstly, the basic calories and protein per kilogram depending on age as for a normal child and, secondly additional requirements depending on the surface area of the burn. With such a programme the weakness of treating all children, whatever their age, on the same formula related only to surface area burn, is overcome. Parenteral nutrition is commenced as soon as the shock phase has been controlled and is continued until enteral intake by gastric tube is sufficient to cover the requirements. Such tube feeding requires the selection of an isotonic liquid diet so as so limit the possibility of diarrhoea. Isocal (Mead Johnson) has been found generally acceptable. Gradually as the patient recovers, oral intake is introduced and the child returns home on a normal nutritional diet, expectantly without weight loss and even with some weight gain, which befits any normal child under treatment for some months. Preburn nutrition, disease and infection, hyperthermia, hypothermia, evaporative water loss, active exercise, psychological well being, social state, early skin cover and limitation of stress are important aspects affecting metabolism and require careful supervision and management. The limitation of metabolism is as important as increasing the caloric intake and this is exemplified at the time of operation, which should be as nonstressful as possible. Every two weeks an adjusted assessment is made of the burned area still to be grafted and the caloric requirements are reduced accordingly. Assessment as to the success of the regime is made upon the results of daily weighing. Extra vitamins and elements are given and blood electrolytes and urine glucose and protein are regularly monitored.
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PMID:Nutrition in the severely burned child. 678 87

A female patient presented with severe hypokalemia and muscle weakness following chronic abuse of laxatives (Folia Sennae). Parenteral substitution of potassium resulted in complete normalisation of the clinical signs and of the pathologically elevated serum concentrations of CPK, LDH and GOT. The importance of laxatives as a possible cause of severe hypokalaemic conditions is underlined by this case report.
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PMID:[Laxative-induced hypokalemic myopathy. A case history]. 693 Jul 55

An outbreak of bacillary haemoglobinuria was recorded in 60 out of 110 sheep in Ludhiana, Punjab, India. The condition was clinically characterised by fever, haemoglobinuria, constipation, weakness of hind quarters followed by recumbency, respiratory distress and death in 16 sheep. Haematological studies revealed moderate to severe degrees of anaemia associated with leucocytosis. Plasma gamma-glutamyl transferase, alkaline phosphatase and creatinine phosphokinase activities were significantly higher in haemoglobinuric sheep. Babesiosis and copper poisoning were ruled out on stained blood film examination and from blood mineral profiles, respectively. Post-mortem examination of affected sheep revealed no gross changes. Pure cultures of Clostridium haemolyticum isolated from heart blood, liver, kidney and spleen of freshly killed sheep confirmed the disease. Parenteral administration of procaine penicillin was effective in the treatment of affected sheep.
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PMID:An outbreak of bacillary haemoglobinuria in sheep in India. 777 Sep 49

Migraine is caused by intermittent brain dysfunction. Attacks result in severe unilateral headache with nausea, vomiting, photophobia, phonophobia and general weakness. The prevalence of migraine is 12 to 20% in women and 8 to 12% in man. Treatment of an acute attack is done by antiemetics in combination with analgesics. Severe migraine attacks are treated with ergotamine or sumatriptan. Parenteral treatment is performed most efficiently and safely with i.v. ASA. Frequent and severe attacks require prophylaxis. Drugs of first choice are metoprolol, propranolol, flunarizine and cyclandelate. Substances of second choice are valproic acid, DHE, pizotifen, methysergide and magnesium. Homeopathic remedies are not superior to placebo. Nonpharmacological treatment consists of sport therapy and muscle relaxation techniques.
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PMID:[Migraine--diagnosis, differential diagnosis and therapy]. 913 7

The most frequent consequence of chronic alcohol intake is a toxic polyneuropathy. It results from inadequate nutrition, mainly deficiency of thiamine and other B vitamins. Additionally there is a direct neurotoxic effect of ethanol. Signs and symptoms are 1. distal sensory disturbances with pain, paresthesia, and numbness in a glove and stockings-pattern, 2. weakness and atrophy of distal muscles, pronounced in the lower limbs, 3. loss of tendon jerks, 4. affection of autonomic fibers. Therapy consists in absolute alcohol abstinence, high-caloric nutrition, parenteral thiamine and other vitamins. Against paresthesia and pain, carbamazepine, salicylates, amitryptiline are effective. Parenteral tioctacid may be tried. The prognosis of alcoholic polyneuropathy is favorable, with alcohol abstinence, within several months up to a few years. In chronic alcoholic patients peripheral nerves frequently are injured by compression during alcohol intoxication. Peroneal nerve lesions result from compression in the region of the neck of the fibula during a prolonged lying position, the radial nerve is injured during sitting with the upper arm placed on the backrest of a bench. Usually pressure palsies resolve spontaneously. Rhabdomyolysis is a rare but life-threatening complication of alcoholic delirium. Symptoms are severe muscle pain, swelling of extremities, pigmenturia. The major complications of rhabdomyolysis are renal and respiratory failure, and cardiac arrhythmias due to electrolyte imbalance. Intensive care is needed with control of hyperkalemia, hydration, alkalinization of urine, hemodialysis if indicated.
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PMID:[Alcohol and the peripheral nervous system]. 1080 76

1. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acid-base balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10-25 ml/min. With glomerular filtration rates below 10 ml/min, there are almost always abnormalites in the body's internal environment with clinical repercussions. 2. Water Balance Disorders: In advanced chronic kidney disease (CKD), the range of urine osmolality progressively approaches plasma osmolality and becomes isostenuric. This manifests clinically as symptoms of nocturia and polyuria, especially in tubulointerstitial kidney diseases. Water overload will result in hyponatremia and a decrease in water intake will lead to hypernatremia. Routine analyses of serum Na levels should be performed in all patients with advanced CKD (Strength of Recommendation C). Except in edematous states, a daily fluid intake of 1.5-2 liters should be recommended (Strength of Recommendation C). Hyponatremia does not usually occur with glomerular filtration rates above 10 ml/min (Strength of Recommendation B). If it occurs, an excessive intake of free water should be considered or nonosmotic release of vasopressin by stimuli such as pain, anesthetics, hypoxemia or hypovolemia, or the use of diuretics. Hypernatremia is less frequent than hyponatremia in CKD. It can occur because of the provision of hypertonic parenteral solutions, or more frequently as a consequence of osmotic diuresis due to inadequate water intake during intercurrent disease, or in some circumstance that limits access to water (obtundation, immobility). 3. Sodium Balance Disorders: In CKD, fractional excretion of sodium increases so that absolute sodium excretion is not modified until glomerular filtration rates below 15 ml/min (Strength of Recommendation B). Total body content of sodium is the main determinant of extracellular volume and therefore disturbances in sodium balance will lead to clinical situations of volume depletion or overload: Volume depletion due to renal sodium loss occurs in abrupt restrictions of salt intake in advanced CKD. It occurs more frequently in certain tubulointerstitial kidney diseases (salt losing nephropathies). Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. The use of diuretics in volume overload in CKD is useful to force natriuresis (Strength of Recommendation B). Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses (Strength of Recommendation B). The combination of thiazides and loop diuretics can be useful in refractory cases (Strength of Recommendation B). Weight and volume should be monitored regularly in the hospitalized patient with CKD (Strength of Recommendation C). 4. Potassium Balance Disorders: In CKD, the ability of the kidneys to excrete potassium decreases proportionally to the loss of glomerular filtration. Stimulation of aldosterone and the increase in intestinal excretion of potassium are the main adaptive mechanisms to maintain potassium homeostasis until glomerular filtration rates of 10 ml/min. The main causes of hyperkalemia in CKD are the following: Use of drugs that alter the ability of the kidneys to excrete potassium: ACEIs, ARBs, NSAIDs, aldosterone antagonists, nonselective beta-blockers, heparin, trimetoprim, calcineurin inhibitors. Determination of serum potassium two weeks after the initiation of treatment with ACEIs/ARBs is recommended (Strength of Recommendation C). Routine use of aldosterone antagonists in advanced CKD is not recommended (Strength of Recommendation C). Abrupt reduction in glomerular filtration rate: Constipation. Prolonged fasting. Metabolic acidosis. A low-potassium diet is recommended with GFR less than 20 ml/min, or GFR less than 50 ml/min if drugs that raise serum potassium are taken (Strength of Recommendation C). In the absence of symptoms or electrocardiographic abnormalities, review of medications, restriction of dietary potassium and use of oral ion exchange resins are usually sufficient therapeutic measures (Strength of Recommendation C). If symptoms and/or electrocardiographic abnormalities are present, the usual parenteral pharmacological measures should be used (10% calcium gluconate, insulin and glucose, salbutamol, resins, diuretics) (Strength of Recommendation A). Parenteral bicarbonate and ion exchange resins in enemas are not recommended as first-line treatment (Strength of Recommendation C). Hemodialysis should be considered in patients with glomerular filtration rates below 10 ml/min (Strength of Recommendation C). 5. Acid-Base Disorders in CKD: Moderate metabolic acidosis (Bic 16-20) mEq/L is common with glomerular filtration rates below 20 ml/min, and favors bone demineralization due to the release of calcium and phosphate from the bone, chronic hyperventilation, and muscular weakness and atrophy. Its treatment consists of administration of sodium bicarbonate, usually orally (0.5-1 mEq/kg/day), with the goal of achieving a serum bicarbonate level of 22-24 mmol/L (Strength of Recommendation C). Limitation of daily protein intake to less than 1 g/kg/day is also useful (Strength of Recommendation C). Use of sevelamer as a phosphate binder aggravates metabolic acidosis since it favors endogenous acid production and therefore acidosis should be monitored and corrected if it occurs (Strength of Recommendation C). Hypocalcemia should always be corrected before metabolic acidosis in CKD (Strength of Recommendation B). Metabolic acidosis is an infrequent disorder and requires exogenous alkali administration (bicarbonate, phosphate binders) or vomiting.
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PMID:[Electrolyte and acid-base balance disorders in advanced chronic kidney disease]. 1901 44

Hypertensive crisis is an acute, life-threatening condition associated with a substantial sudden increase in blood pressure. If the increase is accompanied by a damage of brain, cardiovascular system, eye ground or kidneys, it is referred to as an emergent hypertensive situation. In case of complaints comprising chest pain, shortness of breath, headache, epistaxis, weakness, faintness or seizure alone without organ damage, it is referred to as an urgent hypertensive situation. Treatment of emergent situations is parenteral and is conducted under a permanent monitoring in an intensive care unit. Nitrates, urapidil, diuretics, angiotensin-converting enzyme inhibitors, calcium channel blockers, beta blockers and clonidin are used with respect to organ damage and accompanying diseases. Rate of blood pressure reduction and target values depend on a type of organ damages. An escalation of per oral medication is used in the treatment of urgent situations. Parenteral medication is indicated only in case of failure of this approach.
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PMID:[Hypertensive crisis--the present view]. 1989 22


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