Acute kidney and hepatic failure
Acute renal failure.
Anatomy and physiology.
Kidneys are the pair organs located in the retroperitoneum (at the level of 12-th rib in the loin region). Their main function is elimination of the metabolic waists from the organism. They are supplied with blood by paired renal arteries, which are direct arterial branches of abdominal aorta.
Nephron is the basic functional unit of the kidneys. Its structure is quite complicated: it consists of renal corpuscle (Bowman-Shumlanski’s capsule andglomerulus), proximal convoluted tubule, loop of Henle, distal convoluted tubule and direct tubule.
Kidneys are exclusively “hard-working” organ. Their total weigh is hardly 0,4% of the total body weight, however they receive 25 % of cardiac output. 10% of total inhaled oxygen are used for their metabolic needs. During the day nearly 150 liters of primary urine are ultrafiltrated out of the blood. Ultrafiltration is possible only when effective filtration pressure is not less than 12 mm Hg. It is defined as a difference between hydrostatic (47 mm Hg), oncotic (25 mm Hg) andintracapsular pressure (10 mm Hg).
EFP=Hp(47)-Op(25)-ICp(10)= 12 mm Hg
So when hydrostatic pressure (mean arterial pressure) is decreasing or when intracapsular pressure is reaching critical values filtration stops and renal failure appears.
In tubules water, electrolytes and glucose are reabsorbed and metabolic wastes are secreted to the urine. Eventually during one day only 1 % of primary urine is evacuated from the organism in the form of secondary urine with high concentration of toxic substances.
Kidneys participate in haematopoiesis, regulation of fluid balance, electrolytes metabolism and acid-base balance.
Kidneys are also organs of secretion: their parenchyma produces rennin – substance very important for vascular tone regulation.
Etiology and pathogenesis of acute renal failure (acute kidney injury).
Acute kidney injury is a syndrome appearing due to sudden and progressive affection of nephrones, which causes violation of renal function and induces life-threatening homoeostasis disorders.
The reasons of acute kidney injury are divided into 3 gorups:
1. Prerenal: pathological conditions, which lower renal blood flow, such as hypovolemia, hypotension, thrombosis, renal artery embolism, renal artery spasm, haemolysis, myolysis (muscle desintegration). Thus the prerenal failure can be connected with the massive blood loss, shock (traumatic, anaphylactic,cardiac), dehydration (burns, pancreatitis, peritonitis, vomiting, diarrhoea), crush-syndrome, transfusion of incompatible blood, acute respiratory failure.
2. Intrinsic: the primary damage is caused to the renal parenchyma by exogenous toxins (alcohol surrogates, acetic acid, ethylene glycol, heavy metal salts), nephrotoxic antibiotics (aminoglycosides), bacterial toxins (in case of sepsis), acute glomerulonephritis, eclampsia.
3. Postrenal: acute renal failure appears due to complications of urine outflow (tumours and calculi of renal pelvis and ureter, prostate, accidental ligation of the ureters during operation).
In 70% of the cases acute renal injury appears as a result of prerenal cause. In stress conditions (massive blood loss, multiple injuries) adrenals intensively produce catecholamines: arterioles of skin, smooth muscles, intestines and kidneys spasm. As you probably remember this helps to save the brain and heart (additional blood for circulating blood volume), however for the rest organs this situation, lasting over 3-4 hours will bring ischemia and eveecrosis.
Another mechanism for acute renal failure is connected with the acute vascular insufficiency (collapse, endotoxicosis). Hydrostatic pressure decreases and thus filtration of the blood lowers.
The mechanism of this pathological process is next: hypoperfusion-renal ischemia-hypoxia-coagulation of blood in glomerular vessels-termination of plasma filtration-affection of tubules membranes- compression of the nephron and capillaries-renal necrosis.
Death of over 75% of nephrons finds its clinical manifestation in acute kidneys injury. All the functions of the kidneys- ultrafiltration, reabsorption, secretion, bioactive substances production – are violated.
Stages of acute kidneys injury: clinic and treatment.
Clinically in acute kidneys injury we differentiate 5 stages:
I. First stage (initial) is the stage of shock: depends on the initial aggressive agent and duration of its influence. It can last several hours or several days (2-3). Clinic also depends on the causing factor, however first of all you should observe carefully the haemodynamics and urine output, because correct evaluation of patient’s condition and proper treatment may prevent the development of next stages.
Warring symptoms are:
– arterial hypotension (systolic blood pressure less than 70 mm Hg if it stays during few hours);
– decrease of urine output;
– hyposthenuria (low specific gravity- less than 1006-1008)
Intensive treatment depends on the primary disease. So you have next possibilities:
1. Hypovolemic shock: profuse bleeding, plasma loss, dehydration.
a. restore the circulating blood volume (blood components transfusions, colloids and crystalloids infusions, glucose solutions) – on time provided correction of circulating blood volume (and you will notice it through normalization of blood pressure, pulse, haemoconcentration indexes and especially central venous pressure) – in most cases means restore of the diuresis.
b. if there is no effect of infusion therapy: to liquidate renal arteries spasm and restore microcirculation give α-adrenoceptor antagonists (droperydol,aminazin, ganglionic blockers, epidural anesthesia); stimulate diuresis with 30% mannitol solution 1 g/kg 1/v with the speed 80-100 drops per minute (with 40% glucose solution), 1% furosemid solution (beginning with 2-4 ml every 7-10 minutes and up to 40-50 ml); use additionally spasmolytics (10 ml of 2% euphillinsolution i/v with saline). This “triple shot” combined with infusions can liquidate the functional renal failure.
2. Acute vascular insufficiency: anaphylaxis, toxic collapse, orthostatic collapse caused by overdose of ganglionic agents or α-adrenoceptor antagonists; “warm phase” of bacterial shock; reflectory cardiogenic shock.
a. stabilize vascular tone and perfusion pressure with adrenomimetics (epinephrine, dopamine, mezaton i/v, best of all with infusion pump).
b. use steroids, colloids and crystalloids, steroids and then – stimulate the diuresis (described above).
3. Hemolysis (reactions after blood transfusions, hemolytic poisonings, true drowning in sweet water, some snakebites and insect bites, myolisis during crash-syndrome):
a. increase the circulating blood volume providing hemodilution through infusion therapy;
b. increase blood pH infusing 4% solution of sodium bicarbonate (however don’t forget to control its level);
c. liquidate spasm of renal arteries;
d. stimulate diuresis.
In case of intense hemolysis, injuries with massive muscle disintegration it would be wise to begin preventive hemodyalisis.
4. Renal diseases: normalize hemodynamic indexes, give spasmolytics, stimulate diuresis and use antihypoxic treatment.
5. Postrenal reasons of acute kidneys injury demands immediate consultation of urologist and decision about operative liquidation of urine flow obstruction (insertion of catheters into the bladder, ureters; epicystostomy, prostatectomy, lithotomy, etc.). Do not stimulate urine output with diuretics until the reason of obturation is not removed!!!
Lack of diuretic effects after stimulation states severe organic injury of nephrons and you should make a diagnosis acute renal failure, stage of oligoanuria.
II. Second stage- oligoanuria– lasts from several days to 3 weeks (duration depends on the degree of the damage and regeneration ability of the nephrons). It can manifest as oliguria (urine output less than 500 ml/day) or anuria (urine output less than 50 ml/day).
The severity of this stage is determined with its symptoms:
1. Overhydration: quite often it is caused by iatrogenic reasons – doctors try to “overfill” patient with the water to stimulate diuresis (outdated and dangerous conception!) or simply calculate the daily fluid balance in a wrong way (too “positive” balance).In addition this phase is characterized with intensive catabolism (tissues destruction) and thus excessive endogenous water production (up to 1500 ml/day). Clinical findings: increase of the body weight, circulating blood volume, blood pressure, central venous pressure, peripheral oedema, possibly pulmonary oedema.
2. Electrolytic disorders: hyperkalemia, hypermagnesemia, hypocalcemia. Clinical findings: depression, somnolence, hyporeflexia, respiratory and cardiac disorders.
3. Metabolic acidosis is caused by accumulation of hydrogen ions due to disorders of their renal secretion. Clinical findings: noisy rapid deep breathing (compensatory Kussmaul breathing), vomiting, evident haemodynamic disorders.
4. Uraemic intoxication. Clinical findings: consciousness disorders (up to coma), ammonia breath odour, uraemic polyserositis (pleuritis, pericarditis), ulceration of oesophageal mucous membrane and gastric mucous membrane, diarrhoea.
5. Disorders of synthetic renal function. Clinical findings: anaemia due to erythropoietin deficiency and hypertension (connected with renin-angiotensindisorders).
Intensive treatment.
Your therapeutic tactic will differ a lot in comparing with the previous phase.
1. Fight with overhydration. First of all medical stuff should control carefully body weight gain: ideally correct treatment excludes increase of the weight. Everyday patient loses 400-500 ml of water with respiration. Don’t forget to count water loss with vomiting and diarrhea. Infusion therapy should not exceed this total fluid loss and the only solutions you should use are normal saline and 20-40% glucose solutions (with insulin).
2. Control and treat electrolyte disorders: prescribe calcium chloride or calcium gluconate solutions (40-50 ml of 10% solution intravenously). Calcium acts as potassium and magnesium antagonist and thus lowers their plasma concentrations.
3. Treat metabolic acidosis with 4% sodium bicarbonate solution (up to 400-500 ml per day with acid-base control tests). Normalization of blood pH also normalizes potassium level.
4. Catabolism inhibition: to prevent tissues destruction use anabolic hormones (Nerobol, Retabolil) which prevent muscle disintegration and breakdown of the proteins. This helps to reduce endogenous water production and toxins production. For this purpose we are also using concentrated glucose solutions.
5. To eliminate the wastes from the body there are different methods: enterosorbtion (enterodez, polisorb, activated charcoal, etc.), intestinal lavage(cleansing enemas 4-6 times a day), extracorporeal detoxification methods (hemodyalisis, plasmapheresis, hemosorbtion), peritoneal dialysis.
6. Symptomatic treatment: prescribe hypotensive medicines if necessary, preparations for cardiac support, transfuse washed red blood cells. Prevent infectious complications.
Don’t forget, that in case of acute kidneys injury withdrawal of many drugs is delayed or interrupted and thus accumulation effects are possible!
Hemodialysis is the process of extracorporeal waste products removal with the help of “artificial kidney”. The principle of its work is quite simple: special pump pushes the blood through the tubes to the dialyzer. Dialyzer itself is a system of capillaries, made of semipermeable membrane (kuprofan, cellophane), which are “immersed” into the dializing solution (something chemically very close to plasma). When blood passes through the capillaries dialysis, osmosis andultrafiltration take place. During this process toxic wastes (creatinine, urea, uric acid, phosphates, potassium and hydrogen ions) and excessive water move to thedializing solution. Simultaneously ions of sodium and calcium move from the dializing solution into the blood.
According to the method of blood taking and blood return dialysis is conducted through arterial-venous access or venous-venous access. Aseptic conditions are obligatory; anticoagulants are use in most cases (heparin solution). Average blood speed of 200-250 ml/minute determines duration of dialysis up to 4-5 hours.
Absolute indications to haemodialysis are:
– overhydration (CVP over 15 cm H2O);
– hyperkalaemia (potassium more than 7 mmol/l);
– creatinine more than 0,3 mmol/l;
– decompensated metabolic acidosis (pH<7,2);
– daily growth of urea > 5 mmol/l, urea level over 35 mmol/l.
Contraindications to haemodialysis:
– unstable haemodynamics (blood pressure less than 90 mm Hg);
– haemorrhagic syndrome;
– decompensated cardiac and respiratory insufficiencies;
– CNS damages (stroke, intracranial haematoma).
III. Third stage is a stage of diuretic function restoring. It begins when the daily urine output becomes more than 500 ml and lasts for 3-5 days. Due to regeneration of the glomeruli blood filtration is gradually restored. Tubules epithelium regenerates a bit slower and thus water reabsorption is still inadequate. Diuresisgrowth every day and at the end of this phase reaches 1500-2000 ml per day. However urine has low specific gravity and contains large amount of red blood cells and protein. Hyperkalaemia and uraemic intoxication are still dangerous, because wastes elimination is not adequate.
So the intensive treatment is quite similar to the previous stage. You can change the volume of infusions (but again – control the fluid daily balance). When daily urine output will reach physiologic point of 2-3 liters next stage starts.
IV. Forth stage is a diuretic stage (polyuria). It lasts up to 2 weeks. Daily diuresis increase is 800-1000 ml and daily urine output reaches 7-
Intensive treatment is changed: now your task is to restore the circulating blood volume and lost electrolytes reserves. Correction is made according to the laboratory tests and special formulas.
Gradually concentrating ability of kidneys is returned and diuresis is normalized (specific gravity is normalized, electrolytes are reabsorbed).
V. The fifth stage is a stage of recovery. It takes few months or few years to gain complete recovery and for some patients everything will end with a chronic renal failure. In this stage your task is to prescribe symptomatic treatment, proper diet and resort therapy.
Control tests.
1. What is the normal renal blood flow?
A. 5-10% of circulating blood volume
B. 500 ml/ minute
C. ¼ of cardiac output
D. depends on renal activity
E. 40-50% of cardiac output.
2. During the first stage of acute renal failure you should:
A. begin hemodialysis;
B. provide intensive therapy of shock, normalize microcirculation and stimulate diuresis;
C. stop infusions due to overhydration risk;
D. perform paranephral block;
E. prescribe high doses of furosemide
3. What is a contraindication to hemodialysis?
A. potassium level more than 7,0 mmol/l
B. CVP>13 cm H2O
C. pH<7,2;
D. acute renal failure of III or IV stages;
E. prolonged compression of the kidneys
4. Name the symptom atypical for uraemic intoxication:
A. metabolic alkalosis
B. overhydration
C. azotemia;
D. anemia;
E. hypocalcaemia
5. In case of III stage of acute renal failure you should:
A. obligatory prescribe furosemide
B. give infusions in the rate 5-10 ml/kg
C. treat respiratory alkalosis
D. first of all begin with the dialysis
E. avoid diuretics
6. The forth stage of acute renal failure:
A. is terminal
B. shows overhydration and hyperkalemia;
C. is characterized with potassium ions loss;
D. needs hemodialysis;
E. shows metabolic acidosis and compensated dyspnea.
Task 1.
What medicines should not be used for treatment of patient with the II stage of acute renal failure?
a. mannitol; b. concentrated glucose solutions; c. heparin; d. plasma; e. panangin; f. normal saline; g. calcium chloride; h. enterodez; i. rheopolyglucin j. magnesium chloride; k.nerobol.
Task 2.
Here are the clinical and laboratory findings of the patient, who is suffering from the lack of urine for 5 days:
Creatinine 0,64 mmol/l; potassium 7,1 mmol/l; urea 41 mmol/l; CVP 14,5 cm H2O; blood pressure 170/110 mm Hg; heart rate 96/minute.
What treatment should be prescribed?
Task 3.
One week after restore of the diuresis patient with acute renal failure shows such laboratory results: hematocrit 0,5 l/l, plasma sodium 148 mmol/l, plasma potassium 3 mmol/l, chlorine 98 mmol/l. What is the reason for these changes? What changes should be done in the prescriptions?
Violations of homoeostasis and their correction.
The importance of the water to the organism.
Life on earth was born in the water environment. Water is a universal solvent for all the biochemical processes of the organism. Only in case of stable quantitative and qualitative composition of both intracellular and extra cellular fluids homoeostasis is remained.
The body of an adult human contains 60% of water. Intracellular water makes 40% of the body weight, the water of intercellular space makes 15% of body weight and 5% of body weight are made by the water in the vessels. It is considered that due to unlimited diffusion of water between vessels and extra vascular space the volume of extracellular fluid is 20% of body weight (15%+5%).
Physiologically insignificant amounts of water are distributed beyond the tissues in the body cavities: gastrointestinal tract, cerebral ventricles, joint capsules (nearly 1% of the body weight). However during different pathologic conditions this “third space” can cumulate large amounts of fluid: for example in case ofascites caused by chronic cardiac insufficiency or cirrhosis abdominal cavity contains up to 10 liters of fluid. Peritonitis and intestinal obstructions remove the fluid part of blood from the vessels into the intestinal cavity.
Severe dehydration is extremely dangerous for the patient. Water gets to the body with food and drinks, being absorbed by the mucous membranes of gastro-intestinal tract in total amount of 2-3 liters per day. Additionally in different metabolic transformations of lipids, carbohydrates and proteins nearly 300 of endogenous water are created. Water is evacuated from the body with urine (1,5–
Water balance is regulated through complicated, but reliable mechanisms. Control over water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus, volume receptors of the atrial walls, baroreceptors of carotid sinus, juxtaglomerular apparatus of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst appears and this makes us drink water. At the same time posterior pituitary produces antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood flow aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also decreases diuresis (due to osmosis laws water will move to the more concentrated solution). This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and water is actively removed from the body through the kidneys.
Importance of osmolarity for homoeostasis.
Water sections of the organism (intracellular and extracellular) are divided with semipermeable membrane – cell wall. Water easily penetrates through it according to the laws of osmosis. Osmosis is a movement of water through a partially permeable membrane from the solution with lower concentration to a solution with higher concentration.
Osmotic concentration (osmolarity) is the concentration of active parts in one liter of solution (water). It is defined as a number of miliosmoles per liter(mOsm/l). Normally osmotic concentration of plasma, intracellular and extracellular fluids is equal and varies between 285mOsm/l. This value is one of the most important constants of the organism, because if it changes in one sector the whole fluid of the body will be redistributed (water will move to the environment with higher concentration). Over hydration of one sector will bring dehydration of another. For example, when there is a tissue damage concentration of active osmotic parts increases and water diffuses to this compartment, causing oedema. On the contrary plasma osmolarity decreases, when there is a loss of electrolytes and osmotic concentration of the cellular fluid stays on the previous level. This brings cellular oedema, because water moves through the intracellular space to the cells due to their higher osmotic concentration.
Cerebral oedema appears when the plasma osmolarity is lower than 270 mOsm/l. Activity of central nervous system is violated and hypoosmolar coma occurs. Hyperosmolar coma appears when the plasma osmolarity is over 320 mOsm/l: water leaves the cells and fills the vascular bed and this leads to cellular dehydration. The sensitive to cellular dehydration are the cells of the brain.
Plasma osmolarity is measured with osmometer. The principle of measurement is based on difference in freezing temperature between distillated water and plasma. The higher is the osmolarity (quantity of molecules) the lower is freezing temperature.
Plasma osmotic concentration can be calculated according to the formula:
Osmotic concentration= 1,86*Na+glucose+urea+10,
Plasma osmolarity (osmotic concentration) – mOsm/l
Na- sodium concentration of plasma, mmol/l
Glucose- glucose concentration of the plasma, mmol/l
Urea- urea concentration of the plasma, mmol/l
According to this formula sodium concentration is the main factor influencing plasma osmolarity. Normally sodium concentration is 136-144 mmol/l. Water and electrolytes balance can be violated with external fluid and electrolytes loss, their excessive inflow or wrong distribution.
9.3 Fluid imbalance and principles of its intensive treatment.
Water imbalance is divided into dehydration and overhydration.
Dehydration is caused by:
– excessive perspiration in conditions of high temperature;
– rapid breathing (dyspnea, tachypnea) or artificial ventilation without humidification of the air;
– vomiting, diarrhoea, fistulas;
– blood loss, burns;
– diuretics overdose;
– excessive urine output;
– inadequate enteral and parenteral nutrition or infusion therapy (comatose patients, postoperative care);
– pathological water distribution (“third space” in case of inflammation or injury).
Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds (microcirculation disorders) and low skin temperature; intracellular dehydration is characterized with thirst and consciousness disorders. Laboratory tests show blood concentration: hematocrit, hemoglobinconcentration, protein level and red blood cells concentration increase.
Overhydration appears in case of:
– excessive water consumption, inadequate infusion therapy;
– acute and chronic renal failure, hepatic and cardiac insufficiency;
– disorders of fluid balance regulation;
– low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema, transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and central venous pressure. In case of intracellular overhydration appear additional symptoms: nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the extracellular space (without cellular disorders).Blood tests showhemoconcentration; sodium level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution, glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
VH2O – volume of infusion, l
Htp – patient’s hematocrit, l/l,
BW – body weight, 0,2*BW – volume of extracellular fluid,
0,4– normal hematocrit, l/l,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give 0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
VH2O – water deficiency, l
Nap – plasma sodium, mmol/l
BW – body weight, 0,6*BW volume of general body fluid
140 – physiological plasma sodium concentration
Hypotonic dehydration is characterized with clinical features of extracellular dehydration. Laboratory tests show decrease of sodium and chlorine ions. Those changes cause intracellular movement of the water (intracellular overhydration). Hemoglobin, hematocrit and protein levels are increased. Sodium is lower than 136 mmol/l, osmolarity is lower than 280 mOsm/l.
To treat this type of water imbalance use normal or hypertonic saline and sodium bicarbonate solution (depends on blood pH). Do not use glucose solutions!
The deficiency of electrolytes is calculated according to the formula:
Nad = (140-Nap)*0,2 BW,
Nad – sodium deficiency, mmol
Nap – plasma sodium, mmol/l
BW – body weight, 0,2 BW – volume of extracellular fluid
Isotonic overhydration is caused by excess of the water in the vascular bed and extracellular space; however intracellular homoeostasis is not violated.Hemoglobin is less than 120 g/l, protein level is less than 60 g/l, plasma sodium is 136-144 mmol/l, osmotic concentration is 285-310 mOsm/l.
Treat the reason of imbalance: cardiac failure, liver insufficiency, etc. Prescribe cardiac glycosides, limit salt and water consumption. Give osmotic diuretics (mannitol solution 1,5 g/kg), saluretics (furosemide solution 2 mg/kg), aldosterone antagonists (triamterene – 200 mg), steroids (prednisolone solution 1-2 mg/kg) albumin solution if necessary (0,2-0,3 g/kg).
Hypertonic overhydration is a state of extracellular electrolytes and water excess combined with intracellular dehydration. Blood tests show decrease ofhemoglobin, hematocrit, protein level, however sodium concentration is increased over 144 mmol/l, osmotic concentration is over 310 mOsm/l.
To treat this condition use solutions without electrolytes: glucose with insulin, albumin solutions and prescribe saluretics (furosemide solution), aldosteroneantagonists (spironolactone). If it is necessary perform dialysis and peritoneal dialysis. Do not use crystalloids!
Hypotonic overhydration is a state of extracellular and intracellular water excess. Blood tests show decrease of haemoglobin, hematocrit, proteins, sodium and osmotic concentration. Intensive therapy of this condition includes osmotic diuretics (200-400 ml of 20% mannitol solution), hypertonic solutions (50 ml of 10% saline intravenously), steroids. When it is required use ultrafiltration to remove water excess.
Electrolytes disorders and their treatment
Potassium is a main intracellular cation. Its normal plasma concentration is 3,8-5,1 mmol/l. Daily required amount of potassium is 1 mmol/kg of body weight.
Potassium level less than 3,8 mmol/l is known as kaliopenia. Potassium deficiency is calculated according to the formula:
Kd= (4,5-Kp)*0,6 BW
K- potassium deficiency, mmol;
Kp – potassium level of the patient mmol/l;
0,6*BW – total body water, l.
To treat this state use 7,5% solution of potassium chloride (1ml of this solution contains 1 mmol of potassium). Give it intravenously slowly with glucose and insulin (20-25 ml/hour). You can also prescribe magnesium preparations. Standard solution for kaliopenia treatment is:
10% glucose solution 400 ml
7,5% potassium chloride solution 20 ml
25% magnesium sulphate solution 3 ml
insulin 12 units
Give it intravenously slowly, during one hour. Forced bolus infusion of potassium solutions (10-15 ml) can bring cardiac arrest.
Potassium level over 5,2 mmol/l is a state called hyperkalemia. To treat this condition use calcium gluconate or calcium chloride solutions (10 ml of 10% solution intravenously), glucose and insulin solution, saluretics, steroids, sodium bicarbonate solution. Hyperkalemia over 7 mmol/l is an absolute indication for dialysis.
Sodium is the main extracellular cation. Its normal plasma concentration is 135-155 mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia. This condition is caused by sodium deficiency or water excess. Sodium deficiency is calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap – sodium concentration of the patient mmol/l;
0,2*BW – extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of sodium chloride – your choice will depend on osmotic concentration.
Sodium concentration over 155 mmol/l is a state called hypernatremia. This condition usually appears in case of hypertonic dehydration or hypertonicoverhydration. Treatment was described in the text above.
Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107 mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98 mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld– chlorine deficiency, mmol
Clp – plasma chlorine concentration of the patient, mmol/l
0,2*BW – extracellular fluid volume, l.
To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or 5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l). Intensive therapy of this state includes treatment of the disease, which caused it (decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can also use glucose, albumin solutions and dialysis.
Magnesium is mostly an intracellular cation. Its plasma concentration is 0,8-1,5 mmol/l. Daily requirement of magnesium is 0,3 mmol/kg.
Hypomagnesemia is a state of decreased magnesium concentration: less than 0,8 mmol/l. Magnesium deficiency is calculated according to the formula:
Mgd =(1,0 – Mgp)*0,6BW,
Mgd – magnesium deficiency, mmol
Mgp – plasma magnesium concentration of the patient, mmol/l
0,6*BW – extracellular fluid volume, l.
Use 25% magnesium sulphate solution to treat this state (1 ml of it contains 0,5 mmol of magnesium).
Hypermagnesemia is a state of increased magnesium concentration (more than 1,5 mmol/l). This condition appears usually in case of hyperkalemia and you should treat it as you treat hyperkalemia.
Calcium is one of the extracellular cations. Its normal concentration is 2,35-2,75 mmol/l. Daily requirement of calcium is 0,5 mmol/kg.
Calcium concentration less than 2,35 mmol/l is called hypocalcemia. Calcium deficiency is calculated according to the formula:
Cad = (2,5-Cap)*0,2 BW,
Cad – calcium deficiency, mmol
Clp – plasma calcium concentration of the patient, mmol/l
0,2*BW – extracellular fluid volume, l.
To treat this state use 10% calcium chloride (1 ml of the solution contains 1,1 mmol of calcium), ergocalciferol; in case of convulsions prescribe sedative medicines.
Hypercalcemia is a condition with increased calcium concentration (over 2,75 mmol/l). Treat the disease, which caused it: primary hyperparathyroidism, malignant bone tumors, etc. Additionally use infusion therapy (solutions of glucose with insulin), steroids, dialysis and hemosorbtion.
Acid-base imbalance and its treatment.
There are 2 main types of acid-base imbalance: acidosis and alkalosis.
pH is a decimal logarithm of the reciprocal of the hydrogen ion activity. It shows acid-base state of the blood.
Normal pH of arterial blood is 7,36-7,44. Acid based imbalance is divided according to the pH level into:
pH 7,35-7,21 – subcompensated acidosis
pH < 7,2 – decompensated acidosis
pH 7,45-7,55 – subcompansated alkalosis
pH > 7,56 – decompensated alkalosis
Respiratory part of the acid-base imbalance is characterized with pCO2. Normally pCO2 of arterial blood is 36-44 mm Hg. Hypercapnia (pCO2 increased over 45 mm Hg) is a sign of respiratory acidosis. Hypocapnia (pCO2 less than 35 mm Hg) is a symptom of respiratory alkalosis.
Basis excess index is also a characteristic of metabolic processes. Normally H+ ions produced during metabolic reactions are neutralized with buffer system. BE of arterial blood is 0±1,5. Positive value of BE (with +) is a sign of base excess or plasma acid deficiency (metabolic alkalosis). Negative value of BE (with -) is a symptom of bases deficiency, which is caused by acid neutralization in case of metabolic acidosis.
Respiratory acidosis (hypercapnia) is a condition caused by insufficient elimination of CO2 from the body during hypoventilation. Laboratory tests show:
pH<7,35,
pCO2a > 46 mm Hg
BE – normal values
However when the respiratory acidosis progresses renal compensation fails to maintain normal values and BE gradually increases. In order to improve this condition you should treat acute and chronic respiratory violations. When pCO2 is over 60 mm Hg begin artificial lung ventilation (through the mask or tube; when the necessity of ventilation lasts longer than 3 days – perform tracheostomy).
Respiratory alkalosis (hypocapnia) is usually an effect of hyperventilation, caused by excessive stimulation of respiratory centre (injuries, metabolic acidosis, hyperactive metabolism, etc.) or wrong parameters of mechanical ventilation. Gasometry shows:
pH>7,45,
pCO2a <33 mm Hg
BE < +1,5 mmol/l.
However prolong alkalosis brings decrease of BE due to compensatory retain of H+ ions. To improve this imbalance treat its reason: normalize ventilation parameters; if patients breathing has rate over 40 per minute – sedate the patient, perform the intubation and begin artificial ventilation with normal parameters.
Metabolic acidosis is characterized with absolute and relative increase of H+ ions concentration due to acid accumulation (metabolic disorders, block of acid elimination, excessive acid consumption in case of poisonings, etc.). Laboratory tests show:
pH<7,35,
pCO2a < 35 mm Hg
BE (-3) mmol/l.
Treat the main reason of acid-base disorder: diabetic ketoacidosis, renal insufficiency, poisoning, hyponatremia or hyperchloremia, etc. Normalize pH with 4% sodium bicarbonate solution. Its dose is calculated according to the formula:
V=0,3*BE*BW
V- volume of sodium bicarbonate solution, ml
BE – bases excess with “-”, mmol/l
BW – body weight, kg
Metabolic alkalosis is a condition of absolute and relative decrease of H+ ions concentration. Blood tests show:
pH>7,45,
pCO2a normal or insignificantly increased (compensatory reaction)
BE 3,0 mmol/l.
To treat this condition use “acid” solutions, which contain chlorides (saline, potassium chloride). In case of kaliopenia give potassium solutions.
Respiratory and metabolic imbalances can mix in case of severe decompensated diseases due to failure of compensatory mechanisms. Correct interpretation of these violations is possible only in case of regular and iterative gasometry blood tests.
Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l. Calculate the volume of saline and 7,5% sodium chloride solutioecessary for the treatment of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l. Calculate the volume of 4% potassium chloride solutioecessary for treatment of this condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis “gastric ulcer, complicated with pylorostenosis” has potassium concentration 3 mmol/l, chlorine concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A – 57 mm Hg, BE -4,2 mmol/l. Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration 1,5 mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
Acute liver failure.
Anatomy and physiology.
Liver is the largest internal organ, unpaired triangular gland located in the right upper quadrant of the abdominal cavity, below the diaphragm. It is extremely important to the organism because of the variety of activities it performs. Liver is a digestive gland (produces and excretes bile necessary for lipids consumption), a detoxification centre (microsomal oxidation allows detoxification of exogenous and endogenous toxic substances) and a synthetic center, where proteins, lipids and carbohydrates are metabolized. Liver is also an organ of haematopoiesis and a blood reservoir. Additionally it helps to control acid-base balance.
To provide its metabolic needs with the oxygen organism gives nearly 25% of total consumed oxygen; in case of severe intoxication this number growth up to 40% of the total oxygen. Blood flow of the liver is for 25% provided by hepatic arteries and for 80% by the portal vein. Thus the blood liver receives is poorly oxygenated and any hypoxic condition will bring oxygenation disorders first of all to the tissues of the liver. This evolutionary resulted in unique regeneration abilities of the liver: death of 70% of cells will end up with a failure; however after a certain adaptation period hepatic tissues will restore their quantity and quality.
Acute liver failure: aetiology and pathogenesis.
Acute liver failure is a state of hepatic cells dysfunction, caused by unknown earlier liver disease, resulting in general intoxication, coagulation violations, neurological and mental disorders. Its etiology is usually connected with: viral hepatitis (hepatitis B virus, hepatitis A virus), poisonings (mushrooms, dichlorethane, phosphorus, carbon tetrachloride, arsenic), eclampsia, burn disease, anaesthetic gas, antibiotics, sulfanilamides, massive bacterial pneumonia, cirrhosis, hepatic tumours and metastasis.
Advanced liver failure manifests in coma. Hepatic coma is divided into endogenous (“destructive”, hepatocellular) and exogenous (“shunt”, porto-caval). Toxic damage of 70% of liver cells will cause endogenous coma. In case of liver cirrhosis high portal pressure antagonizes portal blood flow and thus most of the blood moves to the caval venous system and is not detoxified – exogenous coma appears. Clinically we usually observe mixed comas.
Central nervous system in case of lever failure is affected in various ways. Ammonia encephalopathy appears because of violations of uric acid synthesis (it is made from ammonia and without this process ammonia concentration increases several times). Food reach with proteins stimulates ammonia encephalopathy onset, as well as gastrointestinal bleedings, hypnotic medicines and opiates, alcohol, surgeries, infections and metabolic alkalosis. In the CNS tissues false mediators like octopamine, amino acids and their toxic metabolites are accumulated. On the background of hypoproteinemia interstitial edema appears and this brings respiratory hypoxia of tissues. At the same time violated synthesis of enzymes, disordered metabolism of carbohydrates and lipids, metabolic alkalosis withhypokalaemia just advance the encephalopathy.
Clinical findings in case of liver failure.
Liver failure has several forms:
1. Excretory form (disorders are mostly connected with bile production, jaundice is the main characteristic).
2. Vascular form (clinically portal hypertension is the most noticeable).
3. Hepatocellular form (most clinical sings are caused by disorders of synthetic metabolism in liver cells).
According to the duration of the process we define acute and chronic liver failure, according to the compensation level- compensated, subcompensatedand decompensated failure.
Central nervous system is damaged gradually: it begins with precoma and progresses into moderate and deep coma.
Clinical findings:
– skin: jaundice, vascular spiders, “hepatic” palm, extension of small superficial face vessels;
– fever;
– hepatic breath odour, hepatic smell of sweat and urine (this smell occurs due to transformation of methionine into methyl mercaptan);
– digestion disorders (nausea, hiccups, inappetence, smooth red tongue, abdominal pain, meteorism, defecation disorders);
– obstructive and diffuse respiration disorders – hypoxic hypoxia;
– cardiovascular disorders (arterial hypotension, tachycardia, extrasystoles);
– haemorrhagic syndrome, anemia (due to interruption of coagulation factors synthesis and bleeding of gastric or oesophageal erosions and ulcers);
– frequent additional complications: renal failure, hepatorenal syndrome is prognostically dangerous.
If liver failure progresses CNS damage deepens and you can clinically observe: weakness, headache, sluggishness, apathy, inversion of sleep and awakening. Disorientation develops gradually, there is possibility of excitement periods and cramps. You can also find overactive tendon reflexes, foot clonus,Babinski’s sign. One of the most significant symptoms is flapping: trepidation of limbs and face, especially of hands in prone position (arms extended). In case of deepest coma you will see dilated pupils, eyeballs are fixed, tendon reflexes are absent.
Progressive and quick decrease of liver size is a prognostically bad sign. However when the disease is chronic and fibrous changes took place this symptom is not noticed (liver stays enlarged).
Intensive treatment.
The basic principle of liver failure treatment is etiologically aimed therapy: you should treat the reason of the failure. Two other important components are prevention and treatment of liver failure complications during 10-14 days necessary for the regeneration of the hepatocytes.
Necessary treatment measures:
1. Patient should follow strictly bed regiment in isolated ward. Medical stuff should follow aseptic and antiseptic rules.
2. Eliminate animal fats and proteins from the patient’s diet to prevent encephalopathy.
3. Liquidate hepatotoxic factors (hypoxia, hypovolemia, haemorrhagic syndrome, intoxication):
– provide oxygen supply (nasal catheter, face mask with the flow 3-4 l/min); sometimes hyperbaric oxygenation and even intestinal oxygenation (0,2-0,3 ml/kg/min) are possible;
– to increase hepatic blood flow restore the circulating blood volume, improve rheological properties of the blood, restore the peristalsis. To achieve this you should: infuse crystalloids and glucose solutions, spasmolytics, 2 % euphyllin solution (20-30 ml/day). 10% albumin solution (200-300 ml) and mannitol solution (1 g/kg) increase oncotic blood pressure and thus help to prevent interstitial oedema of the liver;
– prevent ulceration of stomach and gastrointestinal bleeding by prescription of famotidine or omeprazole (40 mg twice a day); oesophageal bleedings are stopped with Blackmore probe;
– if you suspect stagnated blood in the intestines – remove it, because otherwise intoxication will get more intense;
– use only “fresh” blood stabilized with heparin for transfusions.
Prevent and treat intoxication with:
– intestinal lavage and enemas;
– antibiotics which are not toxic to the liver (for example ampicillin 1,0 every 4 hours);
– extracorporeal blood detoxification (plasmapheresis, hemosorbtion or hemodialysis; usage of artificial liver or artificial spleen);
– prescribe antagonists of ammonium (40-50 ml of 1% glutamic acid solution with glucose 3 times a day; 2,0 of alfa-arginine solution i/v every 8 hours).
4. To stimulate energetic metabolism in hepatocytes prescribe concentrated glucose solutions (10-20% solutions, up to 5g/kg/day). This will also prevent proteins breakdown and thus wastes accumulation.
5. To stabilize the membranes of the hepatocytes prescribe steroids (10-15 mg/kg of hydrocortisone).
6. To stabilize the energetic exchange and stimulate transportation of the lipids prescribe choline chloride (10 ml of 10% solution with 200 ml of glucose solution after previous atropine admission, twice a day).
7. Additionally prescribe vitamins (ascorbic acid, B1, B2, B6, K, E, B12, folic and nicotinic acids in doses 2-3 times higher than daily needs), cardiac glycosides, panangin, antioxidants (cytochrome c, sodium gamma-hydroxybutyrate).
8. Symptomatic treatment helps to stabilize homoeostasis if not to treat failure itself: if necessary use anticonvulsive medicines, antipyretics, etc.
Control tests.
1. The reason of exogenous liver failure is:
A. acute exogenous poisoning
B. exogenous shock
C. hepatitis B
D. hepatic cirrhosis
E. hyperbilirubinemia
2. The reason of endogenous liver failure is:
A. oesophageal bleeding
B. acute carbon monoxide poisoning
C. infectious shock
D. damage of hepatocytes
E. endocrinological diseases
Task 1.
What is typical for exogenous (a.) and endogenous (b.) liver failure?
a. unconsciousness; b. rapid noisy breathing; c. bleeding varicose veins of oesophagus; d. ascites; e. anaemia f. elevated transaminases; g. acute exogenous poisonings; h. viral hepatitis i. alcohol abuse.
Task 2.
Patience, the patient with liver failure, receives:
a. enteral nutrition reached with proteins; b. oxygenation; c. albumin infusion; d. blood transfusion; e. sodium thiopental for cramps treatment f. steroids g. vitamins h. gentamicin i. diuretics.
Acute poisonings.
Acute poisoning is a chemical injury, which occurs when chemical substance gets to the organism and violates its vital functions. If the substance is aggressive enough and proper treatment is not provided on time poisoning will bring death.
Although there are over 500 toxic substances which may cause acute poisoning, clinical picture is made up of quite similar syndromes. Proper diagnostics of these syndromes allows avoiding life-threatening complications and gets the chance to make correct preliminary conclusions about the nature of poisoning.
8.1 Main clinical syndromes of poisonings.
Affection of central nervous system manifests as excitation or depression of patient’s mental activity. Depression of CNS has different stages: confusion, stupor, spoor and toxic coma. One of the coma’s deepness criteria is reaction of the patient to the painful stimuli (you can also check reaction to smell of ammonium chloride). Lack of reaction is a sign of coma. Don’t live such patient without observation, because his condition is severe and at any moment life-threatening complications may appear: those patients have tendency to bradypnoea up to complete respiratory arrest. Also you should not forget that decreased tone of soft palate and tongue in a supine position will violate patency of the airways and patient can die of asphyxia. In addition comatose condition influences reflexes and lack of swallowing can lead to entrance of saline and gastric contents into the airways (and thus to development of aspiration pneumonia).
Usually CNS depression is caused by excessive alcohol consumption or admission of its surrogates, overdose of neuroleptics, sleeping pills, drugs, sedative medicines, antidepressants and carbon monoxide poisoning. You can remind intensive treatment of comatose patients in the chapter 5.
Some poisoning are followed with acute intoxication psychosis (mental disorders, hallucinations, time and space disorientation, inadequate behavior). This clinical picture you can observe in case of atropine poisoning (and also atropine-like agents: tincture of dope, henbane, amanita) or cocaine, tubazid, antihistaminic drugs and organophosphates poisoning.
In case of psychosis you will have to immobilize patient in the bed for his own good and safety (to avoid injuries both patient’s and those of the stuff). You will also have to do this in order to maintain i/v lines for antidotes and sedative infusions (aggressive patient will try to remove everything he or she considers irritating). Constantly observe the patient’s vital functions.
Toxic affection of the respiratory system can progress as the violation of:
a. external respiration – neurogenic form, aspirations and obstructions of the airways which bring hypoxic hypoxia;
b. hemoglobin’s function – aniline and nitrobenzene create methmoglobin, carbon monoxide connected with hemoglobin creates carboxyhemoglobin and neither the first nor the second is capable of normal oxygen transportation; heavy metal, organic acids and arsenic poisonings lead to destruction of the red blood cells and emission of the free hemoglobin into the plasma;
c. oxygen transportation due to the decrease of circulating blood volume – exotoxic shock;
d. cellular respiration – tissue hypoxia occurs when cytochromes are blocked with toxins like cyanides.
Practically all severe poisonings earlier or later lead to hypoxia, because they violate oxygen supply, transportation and consumption.
Your immediate therapy actions in this situation will be:
– to assess of respiratory system (described above);
– to provide of airways patency (cleaning of the oral cavity, aspiration of the saline and gastric contents, conicotomy if necessary, etc.);
– to begin oxygen supply (face mask, nasal catheter);
– to start artificial ventilation if necessary;
– to prescribe antidotes if they are available (methylene-blue in case of nitro compounds poisonings, unithiolum in case of heavy metals and arsenic poisonings, cytochrome c in case of tissue hypoxia);
– to start hyperbaric oxygenation in case of carbon monoxide poisoning;
– to begin infusion therapy in order to stabilize the hemodynamics;
– to start general detoxification;
– to prescribe symptomatic treatment and provide prevention of the complications (for example prescription of antibiotics).
Affection of the cardiovascular system manifests as inability of the heart and vascular bed to provide adequate blood supply of the organs, which leads to metabolic disorders and in the worst case to death. Severe toxic damage of cardiovascular system brings acute cardiovascular failure: primary toxic collapse,exotoxic shock, secondary somatogenic collapse.
Primary toxic collapse appears in case of massive poison admission, when compensatory mechanisms are not quick enough to resist the chemical aggression. Immediately or minutes after poisoning patients begin to suffer from reduced cardiac output and thus from decreased blood flow in the tissues. Peripheral pulse is weak or absent, blood pressure critically lowers and cardiac arrest can appear. In most cases of primary toxic collapse ambulance is not able to save the life of the patient due to the fulminant development of life-threatening complication. However you should remember that such collapse occurs only in 5 % of the cases.
Exotoxic shock is the reason of death for 70 % of poisoning victims. Violations of hemodynamics on one hand are caused by direct heart and vessels damage and on the other hand by compensatory sympathetic and adrenal reactions. On the background of CNS and gastrointestinal system violations you will observe disorders of systemic hemodynamics and microcirculation: arrhythmias, decrease of blood pressure, central venous pressure, cardiac output and diuresis. The peripheral vascular tone changes: toxins induce spasm or dilation of arterioles with the ischemia of one and hyperemia of other tissues. Depending on the body reaction on intensive treatment shock can be compensated, decompensated reversible and decompensated irreversible.
In case of toxic shock you should:
– get an i/v line (preferably several, including central venous access);
– start infusions of colloids (albumin, rheopolyglucin, hydroxyethylstarch solutions) and crystalloids (saline, glucose solutions, polarizing solution) in order to normalize blood pressure, heart rate and diuresis; sometimes infusion dose is up to 100-150 ml/kg, (7-10 l/day);
– constantly control patient’s condition: monitor the heart action, blood pressure and central venous pressure;
– provide antidote treatment and detoxification; remember that extracorporeal detoxification is possible only after the stabilization of thehemodynamics (systolic blood pressure >90 mm Hg ).
Secondary somatogenic collapse is the reason of death in 25% of the cases. It can occur few days after poisoning, when the toxin is already eliminated from the body, however the tissue changes (in the lungs, liver, kidneys, heart) are irreversible. Necessary treatment: hemodynamics stabilization, improvement of microcirculation, intensive therapy of functional disorders and organic changes (artificial lung ventilation, hemodialysis, cardiac support, etc.).
Toxic affection of gastrointestinal tract.
Usually poisoning provokes usual protective reactions: nausea, vomiting, diarrhoea. Chemically aggressive agents can cause “corrosive” effects: concentrated acids and bases can burn the mucous membrane of oral cavity, oesophagus and stomach (vomit is coloured with blood). Profuse vomiting and diarrhoea bring dehydration, electrolytes loss and acid-base imbalance. Especially rapid those complications appear in children.
After recovery patients with chemical burns of gastrointestinal mucous membranes may suffer from cicatrisation and stenosis of digestive tract.
Be aware of the fact, that intensive usage of narcotic pain killers and sleeping pills can lead to inhibition of peristalsis and thus to constipation and slow elimination of toxins.
Immediate aid actions:
– clean the stomach. If the patient is conscious stimulate vomiting with the pressing on the root of the tongue or with 2-4 liters of slightly salted fluid. Don’t you ever do this in case of chemical burns!
– if you have the skills and possibility insert the stomach probe and evacuate gastric contents with the help of 10-15 liters of water; if necessary give also antidotes through the probe; you can also use probes with several channels;
– after the gastric lavage in order to bind toxins use enterosorbents (activated charcoal for example);
– stimulate stool with saline laxatives (150-200 ml of 33% magnesium sulfate solution) in order to remove connected with the toxin sorbent from the intestines;
– cleansing enemas also help to eliminate toxins from the body.
Toxic affection of liver and kidneys.
This syndrome is caused by primary toxic damage of the liver and kidneys (nephrotoxic and hepatotoxic poisons) or by the secondary disorders of their functions due to violations of blood flow and oxygenation.
Liver is the main detoxification and biotransformation center of the organism, so it takes the “main blow” during intoxication. Intensive detoxification increases metabolic activity and oxygen consumption of the liver several times. Hepatocytes become very sensitive to hypoxia.
Light forms of toxic and hypoxic affections can develop without clinical manifestation. However they will be noticeable in laboratory tests (elevation oftransaminases, bilirubin, phosphates). Severe poisoning will bring to toxic hepatitis and even hepatic coma.
Among the hepatotoxic substances are: heavy metals salts, dichloroethane, ethylene glycol, deadly amanita toxins.
To protect the liver you should:
– eliminate the toxic substance from the gastrointestinal tract;
– give antidotes if they exist (unithiol for heavy metals salts, lipoic acid for deadly amanita);
– prescribe cleansing enemas 2-4 times a day (to prevent intoxication with the wastes accumulated in the intestine);
– use extracorporeal detoxification (hemosorbtion, plasmapheresis, artificial liver);
– provide adequate oxygenation and blood supply of the liver;
– prescribe symptomatic treatment.
Kidneys are very important for the elimination of the poisons circulating in the blood. So in many cases they are also the “target” of the toxin. They can be damaged primary (poison affect their tissues directly) and secondary though the violations of vital functions (for example hemodynamics in case of exotoxicshock). Their condition you can control with the help of urine output per hour, which normally is not less than 0,5 ml/kg.
To prevent the renal failure you should:
– eliminate the poison as soon as possible (gastric lavage and enemas for gastrointestinal tract; hemodialysis, hemosorbtion, plasmapheresis for blood);
– give antidotes if they exist (unithiol for heavy metals salts, sodium bicarbonate for hemolytic poisons, ethylic alcohol for ethylene glycol and methanol);
– treat disorders of hemodynamics (therapy against exotoxic shock);
– stimulate the urine output with the diuretics on the background of previous rehydration: this will allow you to eliminate diluted in the plasma toxins faster and to prevent renal failure; kidney is an organ which functions normally only if works intense;
Clinical observations tell us, that incredibly massive infusions (10-20-30 l/day) with diuresis stimulation really help patient to dilute and eliminate the toxin without kidneys damage.
In case of acute renal failure you should treat the patient according to the principles described in chapter 6.
Ethylic alcohol poisoning.
This type of poisoning appears in case of excessive alcohol consumption. It is one of the most common poisonings, as well as one of the lightest andprognostically the most favourable (organic damage is rare). However combined with comorbidities and complications it becomes one of the first reasons of death in toxicology, so don’t underestimate it.
Alcohol poisoning, unlike drunkenness, has the characteristic signs of intoxication: vomiting, inhibition of CNS, disorders of cardiovascular system and breathing. Patients usually are in comatose condition. Pay attention to their appearance: clothes are untidy, you caotice sings of involuntary urination or defecation. There is alcohol breathing odour. Skin of the face is hyperaemic and dry. Cyanosis is a sign of respiratory insufficiency, grey shade of skin is a symptom of cardiac disorders. Wet skin might be the symptom of hypoglycaemic coma, hypercapnia or organophosphate poisoning, which are “covered” with the obvious clinic of alcohol poisoning. In case of moderate coma vital functions are usually not involved. Pupils are narrowed or dilated, photoreaction is preserved. Objective criterion of alcohol poisoning is alcohol concentration of the blood:
– less than 1,5‰ – light inebriation
– 1,5‰-3,5‰ – moderate inebriation
– 3,5‰ and more – severe inebriation
Lethal concentration of alcohol is 5-6‰.
The most common complications of alcohol poisoning are next:
– obstruction of the airways with the tongue, soft palate or biological fluids (vomit, saline, sputum, blood) in supine position;
– regurgitation of the gastric contents and development of aspiration pneumonia; lethality is nearly 70%;
– head traumas with brain injuries: patients usually fell and hurt themselves; the problem with such injuries is that the clinic of hematoma (subdural, epidural, intracerebtal) is quite often “covered” with alcohol intoxication and this is why you should always remember about the differential diagnostics. To make a correct diagnosis in case of coma you should check the specific symptoms such as anisocoria (there is no poisoning which causes pupil’s asymmetry!), signs of head injury (scratches, bruises, skull deformations, oto-liquorrhea and nasal liquorrhea, nasal and ear bleeding), asymmetric tendon reflexes and muscle tone, disparity between the amount of alcohol and deepness of coma, prolonged unconsciousness (alcohol coma even without proper treatment lasts only 3-4 hours);
– other traumatic injuries (rib fractures which violate external breathing, spleen or liver ruptures with haemorrhagic shock, ruptures of hollow organs with peritonitis; limb fractures);
– compartment syndrome appears when certain enclosed space within the body for several hours suffers from the decreased blood flow (for example when patients spends few hours in one inconvenient position); even when blood supply will be restored necrotic products will continue pathological process through toxic affection of the life-important organs (for example free myoglobin can cause renal failure).
There is always possibility of chronic diseases exacerbations on the background of alcohol poisoning (stroke, myocardial infarction). Remember about the necessity of complete examination (inspection, palpation, percussion and auscultation of undressed patient) of such alcohol victims – it is the only way to find all the “diagnostic mysteries” patients hide!
Intensive treatment:
– evaluate CNS condition (deepness of the coma);
– provide airways patency and adequate respiration (described above; if necessary – intubate the patient and begin artificial ventilation);
– check the cardiovascular system: heart rate, pulse, blood pressure;
– in case of severe hemodynamic disorders provide infusion therapy;
– insert the stomach probe and remove its contents using lavage with water;
– take blood samples and check blood alcohol level (obligatory!);
– prescribe intravenously: 60-80 ml of 40% glucose solution, 60-80 ml of 4% sodium bicarbonate solution, 5-10 ml of 5% ascorbic acid, 1-2 ml of vitamin B1 solution;
– if there are no comorbidities add analeptic solutions i/m (2-3 ml of caffeine or 2 ml of cordiamin);
– in case of severe intoxication begin forced diuresis.
Poisonings with alcohol surrogates.
Patients can be poisoned with: home-distilled vodka,
The most toxic are methyl alcohol and antifreeze (ethylene glycol) – their lethal dose is 60-100 ml. Lower doses cause neuritis of optical nerve and thus blindness (methyl alcohol), acute renal and liver failures (ethylene glycol).
In case of these poisonings detailed anamnesis and blood identification of the poison (gas chromatography) play the most significant role in the diagnostics. However for the prognosis volume of the poisonous fluid, duration of its influence, functional condition of the liver and effectiveness of the antidote therapy and detoxification are the most important.
In the body methanol and ethylene glycol are metabolised according to so called “lethal-synthesis”: during the breakdown of the poison in the liver there are created substances much more toxic than the parent compounds.
Intensive therapy:
1. Gastric lavage with potassium permanganate (oxidizes methyl alcohol).
2. Give antidote: 50 ml of 40% ethylic alcohol solution every 3 hours orally or 100 ml of 5% ethanol solution intravenously slowly combined with glucose solution during 2 days. Antidote will block the process of their biotransformation in the liver until the poisons will not be eliminated from the body.
3. Actively eliminate the poison from the body through repeated gastric lavages, forced diarrhoea, extracorporeal methods of detoxification (hemodialysis, hemosorbtion, plasmapheresis).
4. In order to treat optic neuritis you should perform retrobulbar inject of steroids.
5. Symptomatic treatment.
8.4 Drug poisonings.
In civilized countries these poisoning are the main reason (65-70% of cases) of hospitalization in toxicology units. Usually patients overdose sleeping pills, narcotic painkillers, antihistamine drugs, hypotensive medicines. Among the reasons are suicide tries, drug abuse, toxicomania and accidental overdose due to hectic pace of modern life, etc.
Clinical picture is usually connected with CNS affection. There are phases of somnolence, sleep and coma. Depending on involvement of other systems coma can be complicated or uncomplicated. Usually respiratory complications appear: inspiration centre depression, violations of airways patency due to soft tissues (tongue, soft palate) or biologic fluids (blood, sputum, saline), pneumonia. In 15-20% of cases the poisoning development is complicated with the exotoxicshock. The peculiarities of this shock are next: circulatory disorders with blood stagnation in the pulmonary circuit, toxic affection of the myocardium and decrease of energy metabolism of the organism.
To indicate the poison you should ask relatives and witnesses and check things of the patient (for example you can find medicine packages). Evaluate the size of the pupils: extremely narrowed pupils (“poppy seeds”) are the effect of narcotics admission; narrowed pupils might be the sign of sleeping or sedative medicines overdose; dilated pupils are the symptom of clofelin, antidepressants or neuroleptics administration; wide pupils covering the whole iris are usually the sign of atropine poisoning (or a poisoning with atropine-like substances: dope, henbane, amanita).
Principles of the intensive treatment in the toxicology unit:
– clean the gastrointestinal tract as soon as possible (gastric and intestinal lavage, enterosorbtion, cleansing enemas) and as often as necessary;
– provide adequate respiration (check airways patency);
– in case of comatose patients intubate the trachea and begin artificial ventilation (sometimes it is necessary for weeks);
– control hemodynamics and treat its violations (infusion therapy and adrenergic agonists or antagonists if necessary);
– stimulate diuresis: patients with barbiturate poisoning should be treated with alkaline forced diuresis in order to eliminate the toxin (add to the infusion 400-600 ml of 4% sodium bicarbonate solution and prescribe diuretics);
– use antidotes: naloxone for opiates, pharmacological antagonists for anticholinergic and cholinomimetic agents; don’t you ever prescribe central analeptics for comatose patients with drugs poisoning – cordiamin, caffeine, bemegride , cytiton, lobelinum can cause “cerebral blood flow steeling effect” and thus they deepen the hypoxia of brain cells!
– provide extracorporeal detoxification to eliminate toxins (hemodialysis, hemosorbtion, plasmapheresis);
– prescribe antibiotics for infectious diseases prevention (for example in case of prolonged artificial ventilation);
– symptomatic treatment.
8.5 Alkali and acid poisonings.
These poisonings are among the most severe and difficult to treat. Accidentally or intentionally (suicide) victim can take mineral acids (hydrochloric, sulphuric, nitric acids), organic acids (acetic or oxalic acid), alkali (ammonium chloride, battery fluid, etc.).
When corrosive substance gets into the body along its way inside chemical burn appears: mucous membranes of oral cavity, throat, oesophagus, stomach are injured. Together they make nearly 14-15% of the body surface. Patients suffer from unbearable pain, eating and drinking are disabled. In case of acid burn coagulatioecrosis appears; alkali burn is more severe, because colliquative necrosis penetrates deeper into the tissues ruining the vessels and causing bleedings. Organic acids easily get into the blood. Sometimes chemical substances or their vapours also get into the airways and thus oedema and risk of asphyxia appear.
Usually part of aggressive substance is spilled over the chin and you caotice the burn. Systemic disorders are characterized with exotoxic shock which develops as burn shock (unbearable pain, dehydration, toxic affection of the heart, decrease of cardiac output, spasm of arterioles and microcirculation block). Organic acids also provoke hemolysis of red blood cells: free haemoglobin transforms into hydrochloric haematin and obturates renal tubules, causing acute renal failure.
Intensive treatment principles:
– evaluate patient’s condition: external respiration, consciousness, cardiovascular system;
– adequate pain relief with narcotic painkillers and non-steroidal anti-inflammatory drugs (1-2 ml of 1% morphine solution; 2 ml of 50% analginsolution);
– liquidate the spasm of gastric cardia and oesophagus (1 ml of 0,1% atropine solution i/m, 5 ml of baralgin solution);
– clean the stomach during first 10 hours after poisoning; insert the stomach probe (cover it thickly with Vaseline and don’t push too hard); use water for lavage and don’t try to perform chemical inactivation of the poison, because during the reaction carbon dioxide can exude and acute expansion of the stomach leads to it rupture;
– provide treatment of shock (sometimes up to 10-12 liters/day of infusions);
– in case of organic acids poisonings (acetic acid, oxalic acid get into the blood) give 1500-2000 of 4% sodium bicarbonate solution intravenously slowly with diuretics; these actions will help to remove hemoglobin (released due to red blood cells hemolysis) and thus to prevent acute renal failure;
– in case of obstructive breathing disorders (mucous membrane edema) use steroids (90-120 mg of prednisolone), antihistamine drugs (2 ml of 1% dimedrol solution intravenously), sedative medicines (2 ml of 0,5% diazepam solution); perform tracheostomy or conicotomy if necessary;
– prescribe antibiotics for infectious diseases prevention (for example in case of prolonged artificial ventilation);
– symptomatic treatment.
During the recovering period patient may need surgeries for restoration of gastrointestinal tract: the most common practice is the bouginage of the oesophagus or, if necessary, oesophagus plastic.
8.6. Poisonings with toxic gases.
Among the toxic gases are carbon monoxide, car exhausts, propane and butane, ammoniac gases. The last one is the most toxic: few inhales are enough to cause unconsciousness.
The foundation of the pathology lies within the atypical haemoglobin – carboxyhemoglobin – combination of normal haemoglobin and toxic gas. Oxygen transportation if violated (in case of severe poisonings there are nearly 70-80% of changed haemoglobin) and thus haemic hypoxia appears. In addition within the tissues cytochromes are connected with toxic substances and this leads to tissue hypoxia.
Clinical findings in case of carbon monoxide poisoning depend on the severity of the poisoning. In case of mild intoxication they are: headache, nausea, vomiting. Moderate intoxication shows unconsciousness for 12-16 hours and severe intoxication is characterized with coma, central disorders of breathing, toxic affection of heart and other organs, etc.
If intoxication advances changes of central nervous system become irreversible (brain death is possible).
Intensive treatment.
In case of mild and moderate poisonings you should you should carry the patient out of the toxic atmosphere as soon as possible. In hospital conditions you should provide oxygen supply, get an intravenous line for crystalloids infusion and prescribe vitamins.
In case of severe intoxication begin artificial ventilation with high oxygen flow. Luckily there is an antidote for carbon monoxide poisoning: hyperbaric oxygenation. Connection with oxygen is more natural for haemoglobin and when the pressure of oxygen is higher than its usual partial pressure carbon monoxide is replaced from the haemoglobin. Usually in case of comatose patients 40-50 minutes sessions every 6-12 hours are enough.
To normalize tissue metabolism prescribe antihypoxants: 20% solution of sodium oxybutirate (20-40 mg/kg i/v) and cytochrome c (2-3 ml i/v) every 4-6 hours. To improve microcirculation dilute the blood with crystalloid infusions (check the level of hemodilution with hematocrit – stop when it will reach 0,3-0,35 l/l).
Prevent the infectious complications and brain oedema with standard methods.
8.7 Organophosphate poisonings.
These are the poisonings with insecticides, acaricides, herbicides, fungicides, rodenticides, desiccants, defoliants and with chemical warfare agents such as sorin, soman, V-x.
Organophosphate substances are fats and water soluble and thus they penetrate easily through the skin and mucous membranes (gastrointestinal tract, airways, etc.). In the blood they block an enzyme – cholinesterase – responsible for the breakdown of acetylcholine. As you remember acetylcholine is a universal synaptic mediator of nervous impulses and thus its accumulation on the post-synaptic membranes will cause continuous stimulation of vegetative nervous system and cross-striated muscles.
Clinically you will see: nausea, vomiting, cramps; unconsciousness in severe cases. Sometimes in the place of penetration you can see muscle fasciculation (if the poison was administered orally – tongue twitching). Stimulated parasympathetic nervous system shows wet skin, increased salivation and bronchial secretion (sometimes you can even see white phlegm in the mouth – don’t mistake it with the pink phlegm of pulmonary oedema), narrowed pupils,bradycardia (heart rate 40-30 beats per minute). In addition to the obvious clinic you can always check the environment of the patient for the signs of organophosphate poisons (specific smell, containers with toxins, etc.).
One third of patients suffer from exotoxic shock, which primary causes hypertension and then hypotension, unconsciousness and depression of respiration.
Immediate aid:
– take patient out of the dangerous environment (if you suspect that the mechanism of poisoning is inhalation);
– clean the stomach with large amounts of cold water; repeat it several times, because these substances are excreted through the mucous membranes of gastrointestinal tract;
– give saline laxative;
– if the poison affected skin – wash it with alkaline solution.
Antidotes:
a. use peripheral m-anticholinergic drug – atropine: during the first few hours 2-3 ml of 0,1% atropine solution (up to 30-35 ml during the whole period of intensive atropinization); pay attention to the signs of atropine administration as they are the measure of your antidote treatment effectiveness: termination of excessive bronchial secretion, dilation of the pupils, tachycardia (90-110/min). During next 3-5 days continue atropine prescription (from 10-15 mg to 100-150 mg/day – period of supportive atropinization). Control clinically the level of atropinization.
b. use cholinesterase reactivators: 1-2 ml of 15% dipiroxim solution i/m, up to 600 mg; 3 ml of 40% izonotrozin solution i/m up to 3-
You should also provide usual treatment as soon as possible: infusion therapy, forced diuresis, hemosorbtion, plasmapheresis, hemodialysis and antibiotics for infection preventions.
In case of ineffective external respiration and comatose patient’s condition intubate the patient and start artificial respiration. Convulsions in case of organophosphate poisoning are treated with sodium oxybate (75-100 mg/kg i/v every 4 hours). Cardiac glycosides, calcium chloride, euphillinum are forbidden in case of organophosphate poisonings, because they induce toxic heart affection.
Be aware of the possibility of “second poisoning wave”: even 4-8 days after the stabilization of the patient’s condition clinical picture of the poisoning might return and this time hemodynamics will decompensate quickly.
8.8 Mushroom poisoning.
There are edible, non-edible and relatively edible mushrooms. Non-edible or poisonous mushrooms can contain toxins harmful for central nervous system, liver, kidneys and gastrointestinal tract (according to A. Lokay, 1 968). The most dangerous poisoning is caused by deadly amanita. The poison of this mushroom – amanitotoxin– is not destroyed during cooking and there is no way to detect it in usual conditions. In case of severe poisoning the lethality is 80%.
Specific feature of amanita poisoning is prolonged latent period. Sometimes 6-12 hours pass before the first symptoms of the poisoning appear. All the other relatively edible mushrooms reveal clinical signs of the poisoning much earlier – 1-2 hours after consumption.
After the latent period is over on the background of complete health nausea, profuse vomiting and diarrhoea appear. Those symptoms begin second phase of the poisoning – gastroenterocolitic phase. Liver enlarges; patients suffer from pain in the right subcostal area, weakness, and consciousness disorders. Stool becomes watery and contains mucous. Patients loose up to 4 liters of the fluid during the day. Unlike bacterial food poisonings, mushroom poisonings are not characterized with high fever.
Liver failure and acute kidneys injury are the third phase of the poisoning, which begins on the second or third day of disease. Those failures are characterized with hepatic encephalopathy, jaundice, gastrointestinal bleedings, hepatic breath odour and oligoanuria. The level of alanine and aspartateaminotransferases is very high. When liver returns to its usual size and consciousness is changed into coma hepatargia is stated and prognosis for the disease becomes rather unfavourable.
The forth stage is a stage of recovery and is characterized with gradual regression of the clinical picture and normalization of the laboratory results during several weeks. However survival is possible only for those patients, who ate small amounts of the poisonous mushroom.
Knowing about the high lethality and severity of the amanita poisoning prevention methods become very important. Mushroomers should know the difference between deadly amanita and other mushrooms: deadly amanita is a gill-bearing mushroom with olive or green cap. Its gills white are not connected with the stem. Stem has a bulbus with white volva from one side and a white annulus from another side, under the cap.
Patients should be treated in a special toxicology units or intensive treatment unit. General principles of intensive therapy are:
– gastric and intestinal lavage, enterosorbtion and saline laxatives;
– infusion therapy (necessary to liquidate electrolyte deficiency and provide forced diuresis);
– support of the liver functioning with lipoic or thioctic acid (1000-2000 mg/day), concentrated glucose solutions, steroids (up to 40 mg ofdexamethasone per day) and silibin (50 mg/day);
– extracorporeal detoxification (hemodialysis, hemosorbtion, plasmapheresis, artificial spleen or liver) as soon as possible;
– antibiotics if necessary (penicillin); vitamins (B,C,E);
– external drainage of thoracic duct (decreases intoxication through elimination of toxic lymph).
8.9 Medical operations and manipulations.
Gastric lavage
Indications: necessity to remove poisons or toxins from the stomach, to clean it before operation or to liquidate stagnation during period after the operation.
Equipment required: gastric probe (with two channels if possible), Janet syringe, water for lavage (15-20 liters of room temperature water), gloves and watertight apron.
Procedure: gastric lavage of comatose patients is a procedure for doctors. In our country nurses are not allowed to do this without control of the doctor: unconscious patients have inhibited reflexes and thus probe can be easily inserted into the trachea instead of oesophagus. In this situatioeither cyanosis nor cough may not appear and everything looks just fine, however feeding or lavage try can end with fatal complications (asphyxia and death).
Put on the gloves, choose the probe of necessary size and oil it with Vaseline. Patient should lie on the left side (ask nurse to hold patient’s arms to limit his movements during this unpleasant procedure).
If patient is conscious you can previously use lidocaine spray to anaesthetize mucous membranes. Probe can be inserted through the nose (of course in this case size of the probe is limited) or through the mouse. Don’t push too hard, especially when you are using nasal passage: you can cause bleeding. Ask patient to bow his head to the chest – this will increases chances of correct probe insertion (oesophagus, not trachea). The length of probe you insert can be measured in advance as a distance between earlobe, nose and xiphoid.
Confirmations of correct probe placement:
– auscultate the epigastrium and simultaneously infuse some air with the syringe- you will hear typical “bubble” noises;
– if you made a mistake and probe is in the trachea you caotice air released from the distant end of the tube according to the respiratory movements.
One-time water doe is nearly 200 ml: it will flow out when you will lower the probe or you will have to evacuate the water with the syringe. Repeat these actions until the water wash out the stomach will be clean (usually it takes nearly 10 liters of water).
Forced diuresis.
Indications: intoxications of different origin (poisonings, infectious diseases, endogenous intoxications).
Medicines required: normal saline (3-
Procedure: get and i/v line (central or peripheral) and insert urinary catheter. During the first phase of forced diuresis “water” the patient with crystalloids and detoxification solutions (30-40 ml/kg). During the second phase infuse osmotic diuretics and furosemide solution. Excessive urine output brings potassium loss, which you should treat with polarizing solution. Balance the speed of infusion with the speed of diuresis: generally per 5-7 liters of infused solutions you should receive at least 5 liters of urine.
Constantly control hemodynamics and blood electrolytes.
Control tests.
1. What medicine should be used as an antidote in case of severe soporific drugs poisoning?
A. bemegride
B. cordiamin
C. there is no such meidicine
D. unithiol
E. cytiton
2. What is the most common death reason in case of alcohol poisoning?
A. acute liver failure
B. acute respiratory failure
C. acute renal failure
D. acute heart insufficiency
E. collapse
3. What is necessary for the patient, who took 60 ml of acetic essence?
A. to give 4% sodium bicarbonate solution i/v
B. to clean the stomach with alkaline solution in order to neutralize the acid
C. to use unithiol as an antidote
D. to stimulate intestinal cleansing with saline laxatives
E. central analeptics
4. What is the symptom of organophosphate poisoning?
A. pale and dry skin
B. maximal pupil’s dilation
C. tachycardia
D. muscle fasciculation
E. acute liver failure
5. What is used as an antidote in case of severe carbon monoxide poisoning?
A. cytochrome c
B. cordiamin solution
C. unithiol
D. prednisolone
E. antidotes are not used
6. What is typical for deadly amanita poisonings?
A. first symptoms appear in2-3 hours after mushroom meal;
B. low-grade fever
C. latent period of 6-12 hours
D. first symptoms are haemostatic disorders (bleeding)
E. early unconsciousness
7. What is the necessary aid in case of narcotic painkillers overdose?
A. artificial ventilation
B. cordiamin
C. oxygen supply
D. immobilization of the patient in order to avoid self-injuries during the excitement-phase;
E. cardiac medicines
Task 1.
Patience, the patient of 19 is transported to the ITU by witnesses from the street. Clinical findings: unconscious, cyanotic wet skin, 6 breathes per minute, respiration shallow, blood pressure 70/40 mm Hg, heart rate 112/minute. Name the reason of vital disorder and write the principles of intensive care (algorithm).
Task 2.
Patience, the patient of 19, was found unconscious in his own apartment by the ambulance workers. Clinical findings: total cyanosis, shallow breathing, respiration rate 5/min, pupils extremely narrowed, photoreaction is absent, blood pressure 80/40 mm Hg. In the elbow area there are noticeable signs of injections. Name the reason of vital disorder and write the principles of intensive care (algorithm).
Task 3.
Patience, the patient of 23 was hospitalized into ITU with the diagnosis: mushroom poisoning. It turned out, that yesterday she was eating cooked champignons. 8 hours later she noticed vomiting and diarrhoea. Clinical findings: scleral icterus, dry coated white tongue; painful abdomen (epigastrium and righthypogastric area), painful and enlarged liver (
Write the diagnosis and the phase of the disease.
Task 4.
Patience, the patient of 18, is transported to the toxicology unit with delirium. Clinical findings: hyperaemic face, dry skin, dilated pupils. Blood pressure 140/70 mm Hg, heart rate 127/minute. It is know, that 2 hours ago she took 10 unknown tablets during the suicidal attempt. What is the diagnosis and what are your actions?
Task 5.
Patience, the patient of middle age, was found by the ambulance workers in his own kitchen unconscious. Clinical findings: specific smell of organophosphates in the room, signs of vomit on the clothes, miosis, cold clammy skin with cyanotic shade, foamy white sputum in the mouth, blood pressure 90/50 mm Hg, heart rate 54/minute. What is the diagnosis? What immediate aid should be provided during pre-hospital stage?
Task 6.
Name the reason of the accident and describe the actions of the “Dream team’.
Task 7.
Name the poisoning agent for each antidote: a. atropine, b. unithiol, c. naloxone, d.tetacinum, e. ethylic alcohol, f. dipiroximum, g. lipoic acid?
The essential components of the human cardiovascular system are the heart, blood, and blood vessels. It includes: the pulmonary circulation, a “loop” through the lungs where blood is oxygenated; and the systemic circulation, a “loop” through the rest of the body to provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7 liters) of blood, accounting for approximately 7% of their total body weight.
While it is convenient to describe the flow of the blood through the right side of the heart and then through the left side, it is important to realize that both atria contract at the same time and that both ventricles contract at the same time. The heart works as two pumps, one on the right and one on the left that works simultaneously. The right pump pumps the blood to the lungs or the pulmonary circulation at the same time that the left pump pumps blood to the rest of the body or the systemic circulation. Venous blood from systemic circulation (deoxygenated) enters the right atrium through the superior and inferior vena cava. The right atrium contracts and forces the blood through the tricuspid valve (right atrioventricular valve) and into the right ventricles. The right ventricles contract and force the blood through the pulmonary semilunar valve into the pulmonary trunk and out the pulmonary artery. This takes the blood to the lungs where the blood releases carbon dioxide and receives a new supply of oxygen. The new blood is carried in the pulmonary veins that take it to the left atrium. The left atrium then contracts and forces blood through the left atrioventricular, bicuspid, or mitral, valve into the left ventricle. The left ventricle contracts forcing blood through the aortic semilunar valve into the ascending aorta. It then branches to arteries carrying oxygen rich blood to all parts of the body.
Blood Flow Through Capillaries
From the arterioles, the blood then enters one or more capillaries. The walls of capillaries are so thin and fragile that blood cells can only pass in single file. Inside the capillaries, exchange of oxygen and carbon dioxide takes place. Red blood cells inside the capillary releases their oxygen which passes through the wall and into the surrounding tissue. The tissue then releases waste, such as carbon dioxide, which then passes through the wall and into the red blood cells.
The Circulatory System
The circulatory system is extremely important in sustaining life. It’s proper functioning is responsible for the delivery of oxygen and nutrients to all cells, as well as the removal of carbon dioxide, waste products, maintenance of optimum pH, and the mobility of the elements, proteins and cells, of the immune system. In developed countries, the two leading causes of death, myocardial infarction and stroke are each direct results of an arterial system that has been slowly and progressively compromised by years of deterioration.
Arteries
Arteries are muscular blood vessels that carry blood away from the heart, oxygenated and deoxygenated blood . The pulmonary arteries will carry deoxygenated blood to the lungs and the sytemic arteries will carry oxygenated blood to the rest of the body. Arteries have a thick wall that consists of three layers. The inside layer is called the endothelium, the middle layer is mostly smooth muscle and the outside layer is connective tissue. The artery walls are thick so that when blood enters under pressure the walls can expand.
Arterioles
An arteriole is a small artery that extends and leads to capillaries. Arterioles have thick smooth muscular walls. These smooth muscles are able to contract (causing vessel constriction) and relax (causing vessel dilation). This contracting and relaxing affects blood pressure; the higher number of vessels dilated, the lower blood pressure will be. Arterioles are just visible to the naked eye.
Capillaries
Capillaries are the smallest of a body’s vessels; they connect arteries and veins, and most closely interact with tissues. They are very prevalent in the body; total surface area is about 6,300 square meters. Because of this, no cell is very far from a capillary, no more than 50 micrometers away. The walls of capillaries are composed of a single layer of cells, the endothelium, which is the inner lining of all the vessels. This layer is so thin that molecules such as oxygen, water and lipids can pass through them by diffusion and enter the tissues. Waste products such as carbon dioxide and urea can diffuse back into the blood to be carried away for removal from the body.
The “capillary bed” is the network of capillaries present throughout the body. These beds are able to be “opened” and “closed” at any given time, according to need. This process is called autoregulation and capillary beds usually carry no more than 25% of the amount of blood it could hold at any time. The more metabolically active the cells, the more capillaries it will require to supply nutrients.
Veins
Veins carry blood to the heart. The pulmonary veins will carry oxygenated blood to the heart awhile the systemic veins will carry deoxygenated to the heart. Most of the blood volume is found in the venous system; about 70% at any given time. The veins outer walls have the same three layers as the arteries, differing only because there is a lack of smooth muscle in the inner layer and less connective tissue on the outer layer. Veins have low blood pressure compared to arteries and need the help of skeletal muscles to bring blood back to the heart. Most veins have one-way valves called venous valves to prevent backflow caused by gravity. They also have a thick collagen outer layer, which helps maintain blood pressure and stop blood pooling. If a person is standing still for long periods or is bedridden, blood can accumulates in veins and can cause varicose veins. The hollow internal cavity in which the blood flows is called the lumen. A muscular layer allows veins to contract, which puts more blood into circulation. Veins are used medically as points of access to the blood stream, permitting the withdrawal of blood specimens (venipuncture) for testing purposes, and enabling the infusion of fluid, electrolytes, nutrition, and medications (intravenous delivery).
Venules
A venule is a small vein that allows deoxygenated blood to return from the capillary beds to the larger blood veins, except in the pulmonary circuit were the blood is oxygenated. Venules have three layers; they have the same makeup as arteries with less smooth muscle, making them thinner.
The double circulatory system of blood flow refers to the separate systems of pulmonary circulation and the systemic circulation in amphibians, birds and mammals (including humans.) In contrast, fishes have a single circulation system. For instance, the adult human heart consists of two separated pumps, the right side with the right atrium and ventricle (which pumps deoxygenated blood into the pulmonary circulation), and the left side with the left atrium and ventricle (which pumps oxygenated blood into the systemic circulation). Blood in one circuit has to go through the heart to enter the other circuit. Blood circulates through the body two to three times every minute. In one day, the blood travels a total of 19,000 km (
The Pulmonary Circuit
In the pulmonary circuit, blood is pumped to the lungs from the right ventricle of the heart. It is carried to the lungs via pulmonary arteries. At lungs, oxygen in the alveolae diffuses to the capillaries surrounding the alveolae and carbon dioxide inside the blood diffuses to the alveolae. As a result, blood is oxygenated which is then carried to the heart’s left half -to the left atrium via pulmonary veins. Oxygen rich blood is prepared for the whole organs and tissues of the body. This is important because mitochondria inside the cells should use oxygen to produce energy from the organic compounds.
The Systemic Circuit
The systemic circuit supplies oxygenated blood to the organ system. Oxygenated blood from the lungs is returned to the left atrium, then the ventricle contracts and pumps blood into the aorta. Systemic arteries split from the aorta and direct blood into the capillaries. Cells consume the oxygen and nutrients and add carbon dioxide, wastes, enzymes and hormones. The veins drain the deoxygenated blood from the capillaries and return the blood to the right atrium.
Pic. 4.1 Distribution of blood in the body:
a. hear cavity itself 0 3% (% of blood volume)
b.arteries -15%
c. capillares -12%
d. venous system – 70%
Cardiac cycle is the term used to describe the relaxation and contraction that occur, as a heart works to pump blood through the body. Heart rate is a term used to describe the frequency of the cardiac cycle. It is considered one of the four vital signs. Usually it is calculated as the number of contractions (heart beats) of the heart in one minute and expressed as “beats per minute” (bpm). When resting, the adult human heart beats at about 70 bpm (males) and 75 bpm (females), but this rate varies between people. However, the reference range is nominally between 60 bpm (if less termed bradycardia) and 100 bpm (if greater, termed tachycardia). Resting heart rates can be significantly lower in athletes, and significantly higher in the obese. The body can increase the heart rate in response to a wide variety of conditions in order to increase the cardiac output (the amount of blood ejected by the heart per unit time). Exercise, environmental stressors or psychological stress can cause the heart rate to increase above the resting rate. The pulse is the most straightforward way of measuring the heart rate, but it can be deceptive when some strokes do not lead to much cardiac output. In these cases (as happens in some arrhythmias), the heart rate may be considerably higher than the pulse. Every single ‘beat’ of the heart involves three major stages: atrial systole, ventricular systole and complete cardiac diastole. Throughout the cardiac cycle, the blood pressure increases and decreases. As ventricles contract the pressure rise, causing the AV valves to slam shut.
