Best wishes to The Dynamic Government of Telangana
(and to Dr.C.Laxma Reddy B.H.M.S. , honourable Health Minister of Telangana)
We are sailing in the winds of Thomas Hobbes society, bellum omnium contra omnes. Whatever the cause maybe, the government or economic policies, 20% of people will always suffer.If it goes beyond that , to include 40% or 60% or 80% of people,we have to recheck the policies and their implementation.
What happens, if one of our family members becomes bankrupt, and was forced to enter into a debt trap, a situation which is nothing less than a suicide, just because of a sudden spurt in economy and inflation, which he cannot cope with.
What happens, if one of our family members, who, a breadwinner of the family suffers a sudden illness, and dies helplessly infront of our eyes?
There is a need for everyone to be familiar with the changes in economy and management of health to lead a secure life.
A sudden and arbitrary rise in the “value” of some of the goods and services will lead to evolve a marbled economy with regions of boom separated from regions of slump.The policies which are aimed at “Trickle down Economics” will hamper the economy by exploiting the circulation of currency system and denying the principle of “to each according to their contribution”.
The barter system has given way to currency system with the objective of easy rotation of currency with all walks of life. A sudden rise in the value of some goods and services will hinder the circulation of currency by avoiding some routes of circulation, while overflowing others.
The blocked money which was deliberately kept away from circulation, as black money will affect the common man depending on the quantity of seclusion, and will effect the government depending on the quantity of tax evasion.
Thanks to the BIG MAN and his bold move. It is worthy to be praised, if it is successful, because it hits the target. It is more worthy to be praised, if it is a failure, because it will surface the real problems and the need for rectification – a trial which many countries cannot afford, as it is a global phenomenon.
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This notes is a compilation, useful for the average students like me, to understand some of the concepts of observation of patient suffering with terminal illness, before going to read the standard books.
Declaration of death:
1.Death and the Brain
Clinical Tests : loss of consciousness # absence of spontaneous movements (excluding spinal reflexes) # absence of motor responses in cranial distribution # loss of brainstem reflexes → absent pupillary light reflex-pupils mid-position or greater (‘fixed dilated pupils’) → corneal → gag/pharyngeal → cough/tracheal → vestibulo-ocular (‘cold caloric’) → oculo-cephalic (‘dolls eye’) → loss of capacity to breathe
Laboratory Tests : isoelectric EEG # absent brain blood flow # absence of brain perfusion # absence of cerebral metabolic activity # absent brainstem evoked potentials after wave 1 # evidence of tonsillar herniation by neuro-imaging
(Spinal Reflexes : in brain death* spinal-mediated reflexes include- plantar flexion and triple flexion responses, muscle stretch reflexes, abdominal contractions, sitting up posturing and respiratory-like movements .Brain death requires the use of a supplementary or confirmatory test. The most commonly recommended supplemental tests are EEG, 4 vessel cerebral angiography or radionuclide testing.*Newer tests – inconsistently recommended – include CT angiography, CT perfusion, MR angiography and transcranial Doppler) (Function should be distinguished from activities. Brain function such as the capacity for consciousness or ability for unassisted breathing is distinguished by examples of brain activity such as posterior pituitary antidiuretic hormone release or residual nests of neuronal electrical function)( performance of apnea testing should be reserved as the last test of brainstem function)
2.Death and Circulation
Clinical Tests : absence of palpable pulse * absence of heart sounds * absent breath sounds by auscultation * pulseless electrical activity (non-perfusing rhythm) * isoelectric EKG * absence of breathing * pupils fixed and dilated * no response to pain * loss of pulsatile arterial blood pressure (non-invasive)
Laboratory Tests : absent pulse by audible Doppler * loss of pulsatile arterial blood pressure (invasive intra-arterial line) * echocardiographic absence of aortic valve opening or anterograde circulation * absent pulse oximetry (no oxygen saturation and/or no plethysmography tracing) (The clinical criteria and conditions listed here may not be applicable to neonatal patients (term> 36 weeks, age< 30 days)). (Examples of heart function such as effective contractions of the myocardium leading to anterograde flow of blood through the aorta and arterial system should be distinguished from examples of heart activity such as atrial natriuretic hormone release or residual pulseless electrical activity )
(brain death: irreversible loss of all function of the brain, including the brain stem.* three essential findings in brain death are coma, absence of brain stem reflexes, and apnea.)
1’o clock: Imbalance
2’o clock: Heart and circulation
3’o clock: Lungs
4’o clock: Kidney
5’o clock: Nervous system
6’o clock: Abdomen
7’o clock: Endocrine
8’o clock: Infection
9’o clock: Orthopaedic
10’o clock: Pregnancy
11’o clock: Oncology
12’o clock: Psychiatric & Anaesthesia
1’o clock: Imbalance
o Water ≈50-60% of body weight.(TBW=total body water)
o Water= 2/3rd s intracellular + 1/3rd extracellular
o Water extracellular=intra vascular + interstitial
o Water moves from low solute concentration → high solute concentration
o Hypovolemia = decreased intra vascular volume
o Hypervolemia = increased extracellular volume
o Hypovolemia(decreased intra vascular volume) ĉ decreased extracellular volume
Conditions are – increased fluid losses (GI,polyuria,sweating,burns,haemorrhage), decreased intake of sodium and water, renal sodium wasting, adrenal insufficiency, osmotic diuresis(hyperglycemia),diuretics.
o Hypovolemia(decreased intra vascular volume) ĉ increased or normal extracellular volume conditions are – ascites ,protein loss ,congestive heart failure, increased vascular permeability( sepsis,shock,trauma,burns )
o intra vascular volume=effective arterial volume
o Reduced intra vascular volume stimulates → increased renal sodium reabsorption → increase in total extracellular volume
o intra vascular volume depletion →decreased venous return to the heart →lower stroke volume → sinus tachycardia to maintain cardiac output.
→increased ADH → retention of water
→Hypotension(hypotension & shock →inadequate systemic perfusion ,vasoconstriction(cold skin & extremities)cardiac ischemia, liver & kidney failure)
→diminished urine volume
o Evidence of decreased intra vascular volume: Hypotension, low central venous pressure or pulmonary capillary wedge pressure, tachycardia, oliguria, end- organ dysfunction, peripheral vasoconstriction.
o Hypovolemia requires fluid replacement of, estimated amount of volume depletion over 12-24 hours,in the range of 50-150 ml/hr(200-300ml/hr- if severe volume depletion & organ dysfunction).
o Types of replacement fluids: 1.crystalloid-made of water and small solutes, 2.colloid solutions-consisting of water,electrolytes,and high molecular weight proteins or polymers
o 1.crystalloid≈0.9%NaCl(normal saline), 5% dextrose in 0.9%NaCl, ringers lactate, 5% dextrose in water, 0.45%NaCl, 5% dextrose in 0.45%NaCl
2.colloids≈albumin5%, albumin 25%, 6% hetastarch in 0.9%NaCl
o Replacement of fluid losses from GI tract ≈ 5%dextrose in 0.45%NaCl+kcl (20meq/l) + NaHCO3(45meq/l)
o Hypervolemia(increased extracellular volume) ĉ decreased intra vascular volume conditions- ascites ,protein loss ,congestive heart failure, portal hypertension, excess sodium intake
o Hypervolemia(increased extracellular volume) ĉ increased intra vascular volume conditions-increased sodium retention(renal insufficiency, hyperaldosteronism, hypercortisolism, increased rennin and angiostensin, drugs
o Hypervolemia ĉ decreased intra vascular volume requires diuretic treatment but should be delayed until intra vascular fluid deficit is corrected.
o Hypervolemia ĉ increased intra vascular volume requires diuretics(may also require vasodilators, mechanical ventilator/non invasive positive pressure ventilation).Failure to induce appropriate diuresis may require hemodialysis or ultrafiltration.
o Hypervolemia without change in intra vascular volume requires-1.sodium retention 2.diuretics 3.elimination of extracellular volume( paracentesis, continuous venovenous hemofiltration)
o Water moves from hypotonic (lower osmolality) solution to hypertonic (higher osmolality) solution(osmolality is the concentration of solute in a solution.Ex: plasma osmolality is the sum of concentrations of cations & anions)(urea contributes to osmolality but not tonicity)
o Since sodium is the most abundant extracellular cation,the sum of cation and anion concentrations is approximately 2×(Na+).Hypernatremia always denotes hypertonicity,but hyponatremia may be seen with hypotonicity,normotonicity,or hypertonicity.
o The amount of water that can be excreted in 24 hrs depends on renal concentrating and diluting ability and the quantity of solute excreted per day.
o Urine concentration depends on the amount of ADH(AVP-arginine vasopressin) and renal tubular function.ADH is secreted by posterior pituitary in response to plasma osmolality(↑P.O.→↑ADH, ↓P.O.→↓ADH).(Decreased extracellular volume also stimulates ADH release).Maximum urine concentration(to conserve water excretion) may be limited , if there is renal insufficiency,nephrogenic diabetes insipidus(inadequate response to ADH), & central diabetes incipidus (absence of ADH)
o Failure to dilute urine maximally may result from renal insufficiency,inappropriate secretion of ADH,& adrenal insufficiency(increased permeability of collecting ducts to water)(excess water in the body should be countered by increased volume of maximally diluted urine)
o Normal urine solute excretion≈800 mosm/d, including sodium, potassium, anions, ammonium & urea (urea,breakdown product of amino acids ,makes up about 50% of solute excreted.). Decrease in urine solute excretion(Ex: severely limited protein intake)limits maximum water excretion even if urine is maximally diluted.
o Hyponatremia=plasma sodium<135meq/l, indicates excess total body water for the amount of solute(dilutional hypo natremia)(compensatory mechanism →rapid excretion of water in normal subjects to correct imbalance)
o Hyponatremia ĉ decreased extracellular volume: Normally urinary sodium excretion is low. Increased water intake(thirst) and retention( ↑ADH) leads to ↑TBW relative to the reduced amount of solute. conditions in which ↑sodium and water loss in urine : adrenal insufficiency (lack of cortisol causes collecting ducts excessively permeable to water reabsorption and ADH fails to be suppressed by low P.O.),diuretic use, and salt losing nephropathies.
o Hyponatremia ĉ increased extracellular volume: congestive heart failure ,nephritic syndrome,cirrhosis,protein losing enteropathy,& pregnancy.(oedema, ascites, pulmonary oedema)
o Hyponatremia ĉ Normal extracellular volume: SIADH(syndrome of inappropriate secretion of ADH≈ release of ADH in response to disorders of lung & CNS),decreased solute intake,psychogenic water ingestion.
o Hyponatremia=plasma sodium<135meq/l →altered mental status,(confusion ,lethargy)& seizures . plasma sodium<115meq/l → Hyponatremic encephalopathy (dangerous in patients with acute neurologic disorders-head injury,stroke,haemorrhage).severe Hyponatremia or rapid correction of Hyponatremia leads to osmotic demyelination syndrome(central pontine & extrapontine myelinolysis) →corticospinal and corticobulbar signs,including weakness,spastic quadriparesis,dysphonia, dysphagia & impaired leval of consciousness.
o Low plasma osmolality (<280mosm/kg) confirms hyponatremia owing to increased water relative to solute.(plasma electrolytes,glucose,creatinine,urea nitrogen,urine osmolality,urine sodium,urine creatinine should be measured)
o Diagnosis of SIADH: inappropriately high urine osmolality (300-500mosm/kg)in the presence of low plasma osmolality,and the absence of low urinary sodium concentration.
o Correction of hyponatremia requires administration of normal saline to correct hypovolemia & to increase water excretion. Restriction of water intake(1000-1500ml/day) for asymptomatic Normovolemic hyponatremia .hypertonic saline(3%NaCl) and diuretics for symptomatic or severe hyponatremia.
o Hypernatremia=plasma sodium>145meq/l, always associated with hypertonicity,serum osmolality >300mosm/kg ,indicates a deficit of TBW relative to total body solute. conditions: 1.addition of solute(exogenous-hypertonic saline,sodium bicarbonate, glucose,mannitol etc, endogenous-hyperglycemia by gluconeogenesis,glucogenolysis)( (↑P.O.→↑ADH→minimize water excretion)2.inadequate water intake≈failure to take mandatory intake of 600-700ml/day.3.excessive water loss≈impaired urine concentrating ability.(diuresis, diabetes insipidus) →altered mental status,polyurea
o Water diuresis and solute diuresis can be distinguished by the ratio of urine osmolality to plasma osmolality. solute diuresis=Uosm/Posm>0.9(=osmotic diuresis ĉ isosthenuria) Water diuresis=Uosm/Posm<0.9(ĉ excretion of dilute urine)
o Hypernatremia correction requires1. diuretics and administration of water or 5% dextrose in water –for increased solute.(in renal insufficiency→hemodialysis or ultra filtration with replacement of water,hyperglycemia→intravenous insulin).2.- 5% dextrose in water or 0.45%NaCl –for diminished extracellular volume.3. administration of water orally or 5% dextrose in water I.V-for diabetes insipidus.(central diabetes insipidus→synthetic ADH compounds≈desmopressin)
o Hypokalemia=plasma K+ <3.5meq/l conditions:1.total body potassium is low≈decreased intake(<30-40meq/day),non- renal losses(diarrhoea,sweating),increased renal secretion(increased mineralocorticoids,increased aldosteron,primary hyper aldosteronism),solute diuresis,hypomagnesemia 2.abnormal distribution of potassium between extracellular and intracellular spaces≈drugs and acid-base disturbances,insulin
o Hypokalemia →muscle weakness. Severe Hypokalemia→skeletal muscle paralysis,respiratory muscle weakness,arrhythmias,postural hypotension
o Hypokalemia correction requires oral or I.V.-potassium chloride , potassium phosphate.
o Hyperkalemia= plasma K+ >5meq/l conditions:1. addition of K+ to extra cellular space≈impaired insulin release,rapid K+ administration,rhabdomyolysis,tumor lysis syndrome, 2.impaired disposal of K+ ≈metabolic acidosis,insulin deficiency,beta-blockers use,aldosterone deficiency. Pseudo Hyperkalemia can be seen in extreme thrombocytosis or leukocytosis
o Severe Hyperkalemia →may develop heart block,VF
o Hyperkalemia correction requires-1.intravenous calcium chloride or calcium gluconate(for cardiac conduction system changes)2.insulin+glucose,sodium bicarbonate I.V(for Metabolic acidosis)3.CVVHD
o Hypophosphatemia=plasma phosphorus <2.5mg/dL, severe <1.0 mg/dL. hypophosphatemia always results from a problem of maldistribution of total body phosphorus. Decreased plasma phosphorous and extracellular phosphorus → large quantity of phosphorus in the intracellular space. Should be anticipated in- postoperative patients; in patients with chronic or acute alcoholism, diabetic ketoacidosis, or head trauma; and in patients receiving total parenteral nutrition or mechanical ventilation.Causes-1. Redistribution of Phosphorus ≈ administration of insulin and glucose or acute hyperventilation(treatment of diabetic ketoacidosis and in the refeeding syndrome- as glucose and phosphate move into cells.) Respiratory alkalosis also causes a shift of extracellular phosphorus into cells.2- Decreased intake of phosphorus≈ preexisting diseases leading to decreased dietary intake of calcium, phosphorus, and vitamin D. Binding of phosphorus in the gastrointestinal tract by antacids and specific phosphate-binding compounds prevents absorption.3- increased renal tubular excretion of phosphate≈ subclinical hyperparathyroidism. Clinical consequences of hypophosphatemia are due to decreased production of ATP and erythrocyte 2,3-DPG → Impaired function of skeletal muscles, including respiratory muscles, and myocardium
o Hypophosphatemia correction requires→ Intravenous phosphate is given as sodium or potassium phosphate. Rapid phosphate shifts during treatment, may resolve or worsen the problem. Therefore, close monitoring of plasma phosphorus and other electrolytes is necessary during repletion. . Adult patients receiving parenteral hyperalimentation generally require about 1 g phosphorus daily. Routine repletion of phosphorus in patients with diabetic ketoacidosis has been recommended.
o Hyperphosphatemia= Plasma phosphorus >5 mg/dL. acute elevation can have consequences owing to precipitation of calcium phosphate salts in the heart, kidneys, and lungs, rarely, acute cardiac conduction disturbances. Calcium phosphate precipitation results in acute hypocalcemia. Severe hyperphosphatemia is seen when there is massive tissue breakdown.Causes-1. Impaired Phosphate Excretion- chronic renal insufficiency, hypoparathyroidism(Normal cell turnover releases a steady quantity of phosphorus into the extracellular space that is taken back up into the cells or bone or excreted by the kidney).2- Redistribution of Phosphorus≈ massive tissue breakdown- rhabdomyolysis from trauma or other muscle injury from infection, drugs, seizures, or metabolic problems. Tumor lysis syndrome is seen after chemo or radiotherapy of highly responsive tumors (eg, lymphoma).3- Excessive replacement of phosphorus
o Hyperphosphatemia correction requires→ normal saline infusion in patients who can tolerate this treatment will enhance phosphate excretion, Orally administered phosphate binders. Dietary phosphorus can be minimized by prescribing a low-protein diet and avoiding dairy products that contain both calcium and phosphorus
o Hypomagnesemia= plasma magnesium concentration of less than 1.7 mg/dL, but about 25% of plasma magnesium is bound to albumin. While the plasma level reflects both bound and unbound magnesium, the clinical effects of magnesium, like those of calcium, are due to the unbound ion.Causes-1. Decreased intake, intestinal causes of malnutrition interfere with its absorption.2. Increased losses of magnesium≈ renal magnesium wasting. Hypomagnesemia is also found in association with diabetes mellitus, phosphate depletion, hyperparathyroidism, and thyrotoxicosis. Hypomagnesemia occurring with acute myocardial infarction → ventricular arrhythmias. Cardiac arrhythmias are the most important complications of hypomagnesemia. Hypocalcemia is strongly associated with hypomagnesemia. Tetany, positive Chvostek and Trousseau signs, seizures, weakness, and altered mental status may be seen. Disorder should be anticipated in certain high-risk groups, that is, patients with hypocalcemia, acute myocardial infarction, congestive heart failure, alcoholism, acute pancreatitis, mal-nutrition, diarrhea, or seizures and those receiving diuretics, amphotericin B, or aminoglycosides. . Hypomagnesemia is seen in a large percentage of those with hypokalemia. Refractory potassium deficiency results because administered potassium is unable to enter cells readily and therefore is excreted in the urine. Hypomagnesemia also stimulates renin release and thereby increases aldosterone, further enhancing potassium excretion. Hypomagnesemia is also strongly linked with hypocalcemia and inappropriately low levels of parathyroid hormone.
o Hypomagnesemia correction requires→ Intravenous magnesium sulfate (MgSO4) can be given as 50% solution added to D5W or normal saline.
o Hypermagnesemia≈ Plasma [Mg2+] >2.7 mg/dL: usually asymptomatic, Plasma [Mg2+] >7 mg/dL: weakness, loss of deep tendon reflexes, and paralysis, Plasma [Mg2+] >10 mg/dL: hypotension and cardiac arrhythmias.-Causes-1. Increased intake(Magnesium-containing antacids and laxatives)2. impaired renal magnesiu