Ministry of health of Ukraine

FIRST AID renal failure

1. Background:

Relevance of kidney failure in children due to birth defects, sudden and progressive damage nephrons, resulting impaired renal function and body homeostasis disorders accompanied by the threat of his life.

2. Specific objectives:

1. Analyze the list of defects, diseases and patolohichchnyh conditions that cause kidney failure in children.
2. Explain the major clinical manifestations of renal failure in children.
3. Differentiate renal failure in children depending on the stage of the disease and causes.
4. Interpret helper methods: ultrasound, x-ray, laboratory and biochemical analyzes, hemodynamic parameters.
5. Demonstrate a bladder catheterization technique.
6. Identify features of acute and chronic renal failure.
7. Justify and formulate preliminary clinical diagnosis.
8. Submit algorithm Action physician in acute and chronic renal failure in children.
9. To interpret the general principles of treatment of acute and chronic renal failure in children.

4.2. Theoretical question for the class:

1. Present a etiologic structure of acute renal failure in children.
2. Pathogenesis of acute and chronic renal failure.
3. Know the clinical picture of acute and chronic renal failure.
4. Know the principles of the use of auxiliary examination methods and interpretation of the data obtained in this pathology.
5. Directions of the treatment of acute renal failure in children.
6. Definition tactics sick child after acute renal failure and chronic renal failure.

4.3. Practical work carried out in class (level III digestion).

1. Collect medical history, including information about pregnancy and childbirth relatively specific patient.
2. Conduct review of a sick child, palpation, auscultation.
3. Describe the objective status and determine the clinical and radiological symptoms of acute renal failure.
4. Settle and make a plan examination and treatment.
5. Perform and know the technique a bladder catheterization in children.
CONTENTS TOPICS
"Acute renal NEDOSTATANIST IN CHILDREN"
Kidneys - paired organ located in the lumbar region (at 12 ribs) and acts as a detoxification of the body. Blood supply of the kidneys performed arteries that branch off directly from the abdominal aorta. The basic functional unit of the kidney - the nephron. It consists of a capsule Shymlanskaya-Bowman, covering vascular glomerulus, convoluted tubules, loops of Henle, straight tubules. Kidneys - extremely "efficient" body. With their weight, which is 0.4% of body weight on organ blood flow accounted for 25% of cardiac output. Metabolic processes in the kidney followed by using 10% of oxygen necessary for the functioning of the body.
By reducing the hydrostatic (mean arterial pressure) or with increasing vnutrishnokapsulyarnoho the critical filtration stops developing renal failure.
In the process of renal tubule reabsorption of water, electrolytes, and other substances, and secretion. Eventually excreted about 1% of the urine, now secondary, which contains high concentrations of slag.
The kidneys are involved in hematopoiesis, regulation of fluid and electrolyte status and acid-base balance. Kidney - more and secretory organ. Its parenchyma synthesized renin, which plays an important role in shaping the tone of blood vessels (blood pressure).

Etiology and pathogenesis of acute renal failure

In acute renal failure following factors lead.
1. Prerenal. This includes pathological conditions that lead to a decrease in renal blood flow reduction of BCC, lowering blood pressure, thrombosis, embolism or prolonged spasm of the renal arteries, the disintegration of red blood cells (hemolysis) and muscles (mioliz). The most common reasons they have massive blood loss, traumatic, anaphylactic, cardiogenic shock, loss of plasma hipohidratatsiya with significant burns, pancreatitis, peritonitis, fistulas of the gastrointestinal tract, vomiting and diarrhea, incompatible blood transfusion, prolonged crushing syndrome, acute respiratory failure.
2. Renal. In patients with primary damage occurs when kidney parenchyma of her exogenous poisons (ethylene glycol, formaldehyde, acetic acid, salts of heavy metals), nephrotoxic antibiotics (aminoglycosides), bacterial toxins (sepsis), acute glomerulonephritis, eclampsia pregnancy. Also, this group includes congenital malformations of kidney in children.
3. Postrenalni. Acute renal failure develops as a result of violation of the outflow of urine (tumor and calculus renal pelvis and ureter, prostatic adenoma cancer, ureteral ligation wrong during operations on the pelvis).
In 70% of cases of acute renal failure caused by prerenal pathology. Under critical conditions (massive blood loss, hypovolemia, significant long-term stress) adrenal glands, a large amount of catecholamines. There spasm of arterioles skin, muscle, intestine, kidney arteries. Reduced blood flow in these tissues allows additionally remove a certain amount of blood to maintain tsyrkulyuyuchiyi activities, primarily the heart and brain. Appropriate, from the standpoint of the whole organism, such centralization of circulation with prolonged duration (more than 3-4 hours) causes death of the kidney.
Another mechanism of renal failure occurs in acute vascular failure (collapse, endotoxemia). This dramatically decreases the hydrostatic pressure, which is accompanied by breach of ultrafiltration of blood and damage nephrons.
Hypoperfusion - renal ischemia - hypoxia - clotting of blood in the capillaries of the glomeruli - the cessation of filtration plasma - membrane tubules injury - compression nephrons and capillaries - nefronekroz - this scheme of the pathological process.
The death of 75% of nephrons clinically manifested acute renal failure. Violated all renal function: ultrafiltration, reabsorption, secretion, synthesis of substances.
Stages in the course of acute renal
FAILURE, Distinctive clinical and intensive care
In the clinical course of acute renal failure are five stages.
The first stage (shock). Determine the period of aggressive factor. It lasts from a few hours to 2 - 3 days. Clinical picture painted symptoms of the underlying disease. In the diagnosis of this stage is necessary to investigate the state of hemodynamics and urine output, because the timely and proper conduct of intensive therapy can not prevent the other stages.
Troubling indicators are:
- Hypotension (systolic blood pressure below 70 mmHg, not stabilized within a few hours), decreased urine output (<30 ml / hr.)
- Hipostenuriya (urine specific gravity <1006 - 1008).
Tactics intensive care patients determined considering the causes of pathology. Here are the possible options.
1. Shock, accompanied by absolute hypovolemia (loss of blood, plasma, hipohidratatsiya).
Algorithm intensive care:
a) to restore blood volume (transfusion odnohrupnoyi compatible blood components, the means of hemodynamic, crystalloids and salt-free solutions). Timely recovery of BCC, as evidenced by normalization AT, pulse, hemokontsentratsiynyh indicators, and especially important - CVP - usually accompanied by a reduction in urine output.
b) in the absence of diuretic effect - to relieve vasospasm renal microcirculation recovery advisable to use drugs that exhibit a-adrenolytic action (Mr. droperidol, aminazine) hanhliolityky, epidural anesthesia, stimulate diuresis. Apply 30% Mr. mannitol in 40% of the district of glucose (1 g / kg intravenously at a speed of 80-100 drops per minute), against the background of his actions administered saluretics (furosemide in increasing doses - starting with 2-4 ml 1% solution, every 7th min. - up to 40-50 ml). Complement stimulating introduction to Mr. aminophylline (2.4% district, 10 ml intravenously, dissolved beforehand in isotonic sodium chloride solution). Combined use of these drugs on the background of previous water load (so-called "triple blow") can be eliminated functional renal failure.
2. Conditions involving acute vascular insufficiency (anaphylactic shock, toxigenic, orthostatic collapse, poisoning or ganglioplegic a-adrenolytic intermediaries, "heat" hypotensive phase of infectious-toxic shock, cardiogenic shock reflex).
    Stabilization of vascular tone and normalization of perfusion pressure in these cases reach using agonists (epinephrine hydrochloride mezatona, dopamine - intravenously). These patients also need to perform infusion therapy hemodynamic means as applied glucocorticoids. The next stage of treatment - stimulation of diuresis.
3. Hemolysis (at posttransfuzionnyh reactions, poisoning haemolytic substances "real" drowning in fresh water, bites of some species of snakes and insects) mioliz (the syndrome of long squash). Medical treatment:
a) make infusion therapy for a significant increase in CBV (mode hemodilution);
b) at the same time constantly "oluzhnyuvaty" blood, using a drip 4% Mr. sodium bicarbonate (pH controlled to that of the upper limit of normal);
c) remove the spasm of the renal vessels;
d) stimulate diuresis.
At a massive hemolysis, trauma to destruction of soft tissue earliest expedient to hold sessions hemodializnoyi therapy.
4. In renal disease should also seek normalization of hemodynamic enter antispasmodics, stimulate diuresis and apply antihy therapy.
5. Postrenalna cause kidney failure requires immediate intervention urologist and the issue of the elimination of obstacles outflow of urine (bladder catheterization, ureteral epitsystostomiya, adenomectomy, litotomiya etc.). Stimulate diuresis diuretic purpose to restore the flow of urine is contraindicated!
No diuretic effect on the ongoing intensive therapy shows gross organic changes nephrons. Establish diagnosis of acute renal failure in stage oligoanuria.
The second stage - oligoanuria. It lasts from several days to three weeks, which is determined by the degree of destruction of nephrons and their ability to regenerate. Occurs in the form of oliguria (urine output <500 mL / day) or anuria (urine output <50 ml / day). Severity determined by the development of pathological syndromes:
1) hydration. Often due to iatrogenic causes (the doctor seeks to stimulate kidney activity holding water load, which now contraindicated, sometimes incorrectly calculates daily volume infusion therapy, significantly increasing her). In addition, at this stage in the process of intense catabolism (tissue decay) produced large amounts of endogenous water
(Up to 1500 mg / day).
In patients with marked increase in body weight, CBV, arterial and central venous pressures, the emergence of peripheral edema, pulmonary edema.
2) Disorders of electrolyte balance - hyperkalemia, hypermagnesemia, hypocalcemia.
Clinical symptoms: depression, lethargy, hyporeflexia, respiratory disorders and heart activity.
3) metabolic acidosis. Conditioned by the accumulation of hydrogen ions by disrupting their breeding kidneys.
Patients progressing noisy, frequent, deep breathing (Kussmaul type) compensatory nature, vomiting become more pronounced hemodynamic disorders.
4) uremic intoxication.
Characteristic signs of intoxication is impaired consciousness (up to coma), ammonia breath uremic polyserositis (pleurisy, pericarditis) zvyrazkuvannya lining of the esophagus, stomach, and diarrhea.
5) Synthetic renal disorders.
For patients characterized by anemia (due to dysfunction krovetvorennya) and hypertension (renin-angiotensin origin).
Intensive care.
The therapeutic approach at this stage, unlike the previous one, is changing. It no longer depends on the etiological factors and made taking into account pathological them ¬ syndromes developing in this pathology.
1. Fighting excessive hydration. The patient must be on a special bed - scales. His daily weighed. Proper management of the patient excludes increasing weight. When breathing and through the skin of a patient loses about 400-500 ml of water. Counts fluid loss in other ways (with vomiting, with diarrhea). Infusion therapy should not exceed the amount of the loss, and, as the means of infusion used only Mr. sodium bicarbonate and concentrated (20 - 40%) districts glucose with insulin.
2. Correction of electrolyte imbalance. Administered in large doses of calcium chloride or gluconate (up to 40-50 ml of 10% solution per day) intravenously. How antagonist potassium and magnesium it reduces dangerous concentration of plasma.
3. Treatment of metabolic acidosis. Apply 4% sodium bicarbonate solution, to 300 - 400 ml per day, taking into account the acidity of the blood. Alkalises blood also reduces hyperkalemia.
4. Warning disintegration of tissues. Assign hormones anabolic action (Nerobolum, retabolil) that, reducing catabolism, reduce the breakdown of proteins. Formed less toxins and endogenous water. With the same purpose, use concentrated districts glucose.
5. For detoxification of the body can be used enterosorption (coal NCS enterodezom, polisorb etc.), frequent bowel lavage (cleansing enemas for 4 - 6 times zadobu), extracorporeal detoxification methods (hemodialysis, plasmapheresis, hemodialysis and limfosorbtsiya), peritoneal dialysis.
6. Symptomatic therapy. If necessary, the patient is prescribed antihypertensive the means, heart medications, washed red blood cells transfused. Important role in providing combat hypoxia, prevention of infectious complications.
We're aware of the potential effect of drugs kumulyatsiynoho a violation of their removal from the body of the affected kidney!
Hemodializna therapy - blood purification device using "artificial kidney". How it works: using a special pump roller type tube on highways moves blood from the patient to the dialyzer. Dialyzer is a system of capillaries made of semipermeable membrane (kuprofanu or cellophane) that washed dializuyuchoyu fluid. The chemical composition of the fluid meets dializuyucha plasma. When passing blood through capillaries dialyzer processes of dialysis, osmosis and ultrafiltration. This toxic substances (creatinine, urea, uric acid, phosphate, potassium ions, hydrogen), and excess water from the blood to pass through the membrane in dializuyuchyy solution. Simultaneously dializuyuchoho solution in blood permischuyutsya those ions (sodium, calcium) that are lacking in the patient, aligning the chemical composition of the blood.
Depending on how the collection of blood and infusion therapy patient hemodializnu spend arterio-venous or veno-venous access in aseptic conditions, after previous administration of anticoagulant (heparin district). At a speed of transmission of blood on the highway 200-250 ml per minute playing session hemodializnoyi therapy is usually 4-5 hours.
Absolute indications for hemodializnoyi therapy:
- Hyperhydration body (CVP> 150 mm water column);
- Hiperkaliyplazmiya (plasma K +> 7 mmol / l);
- Creatinine levels> 0.7 mmol / l;
- Daily increase urea> 5 mmol / l;
- Decompensated metabolic acidosis (blood pH <7.2).
- Hemodialysis is contraindicated in:
- Unstable hemodynamic (AT syst. Below 90 mm Hg);
- Haemorrhagic syndrome;
- Decompensation of the cardiovascular and respiratory systems;
- CNS (stroke, intracranial hematoma).
The third stage - the restoration of diuresis. It begins with the selection of more than 500 ml of urine, and lasts up to 3-5 days. Because regeneration glomerular filtration mechanism gradually restored blood. Tubular epithelium regenerates later because reabsorption is still broken. Every day increases urine output - up to 1500-2000 ml. However, the urine has a low specific gravity, contains a lot of protein and erythro ¬ tsytiv. Slag poorly excreted, so still a significant risk to the patient of hyperkalemia and uremia.
This requires the use of pre-treatment strategy. Slightly increase the volume of infusion therapy in accordance with losses. Restoration to the physiological diuresis volume (2-3 liters) determines the transition to the next stage of ARF.
Fourth stage - polyuria. It lasts up to 2 weeks. Daily gains of 800-1000 ml of urine, and urine output - up to 7-9 liters per day. In patients with normal azotemia, dehydration develops simultaneously in a large number of lost potassium and magnesium, which may pose a threat to patients.
Therapeutic tactics must change again: spend massive infusion therapy including losses transfused Canadians liyvmisni solutions. Correction of electrolyte disorders performed according to laboratory measurements on known formulas.
Gradually reduced concentration ability of the kidneys, increasing the proportion of urine, urine output normalized.
Fifth stage - vyzdorovlennya. This process takes from several months to 1-2 years. At this time spend symptomatic therapy, diet therapy and spa treatment.

Materials for self-

Situatsiyne task
Task 1. Woman '15 came with complaints of abdominal pain and lumbar region, fever, vomiting, loss of appetite. In history operated in Connected with bilateral hydronephrosis complicated by chronic pyiyelonefrytom. Pasternatsky positive. In Urinalysis - protein - 0.066 g / l, WBC - 30-40, erythrocytes - 1-2 in sight bakteriyiuriya. In biochemical surveyed increased numbers of urea and creatinine, renography with reduced function of both kidneys to 70%.
1. What is the cause of kidney failure?
2. What treatments might be used?
Answers:
1. Bilateral hydronephrosis, chronic pyiyelonefrytom.
2. Methods of detoxification hemodialysis

Task 2. The boy's mother 13 years after his recovery from the flu celebrates another rise in temperature to 380 - 390 C for 5 days, headache, nausea, weakness in the lumbar constant pulling pain, frequent urination, especially at night, muddy urine, blood pressure 140/80 mm. Hg. century. Pasternatsky positive left and negative right hand side. Preliminary diagnosis of pyelonephritis.

1. What method radiodiagnostics most informative to identify the degree of renal dysfunction?
2. What complication occurred in a child?
Answers:
1. Dynamic renostsyntyhrafiya.
2. Hypertension.
Problem 3. Boy '10 suffering from chronic glomerulonephritis with a 5-year-olds. During the last month - pallor, many "sintsiv" on hands and feet, irritability. On examination severe condition, the child in sopor, leather with ekterychnym shade postoznist the lower limbs, mouth - the smell of ammonia. Breathing deep, noisy, 28 with 1 min. BP - 160/90 mm Hg. century. Cardiac muffled, 110 for 1 min., Arrhythmia, on top and at \ / point - systolic murmur. Liver to 3 cm appears from under the costal arch. By last night urination 1 times, identified 180 ml of urine.
1. Your preliminary diagnosis?
2. What biochemical indicators help clarify the diagnosis?
Answers:
1. Chronic glomerulonephritis, chronic renal insufficiency II degree
2. Increasing numbers of residual nitrogen, urea, kreatenynu; violation electrolyte composition.

Problem 4. 12-year-old child after suffering glomerulonephritis 2 years ago complained of fatigue, weakness, loss of appetite, headache, nausea, thirst, polyuria. The child behind in physical development. OBJECTIVE: leather pale and dry. BH 30/hv, HR 108/hv. Abdomen - soft, epigastric pain, liver + 1.5 cm painful. Pasternatsky weakly positive on both sides. Laboratory studies: normochromic anemia, urea content in blood serum - 8.8 mmol / L, creatinine - 0.18 mg / dL, hyperkalemia, hypermagnesemia, hypocalcemia.

1. Enter the diagnosis?
2. What method to confirm the diagnosis?
Answers:
1. Chronic renal failure.
2. Nefrosyntihrafiya.

Problem 5. Girl 7 years, 2 weeks ago held transplantation humerus due to congenital cystic dysplasia. Immunosupresyvnu received no therapy. Parents viewed Fades odutlovatosti face pastoznost legs, abdomen, reducing urine output. Examination: in Al. Blood Lake. - 11.8 h109 / l, ESR - 22 mm / h., Total protein - 49 g / l, albumin - 32 g / l cholesterol - 4.6 mmol / l. In en. Urine: the relative density - 1031, protein - 4.5 g / l Lake. - 5-6 in sight, er. - 1-2 in sight, cylinders - 1-2 in sight. Daily urine output - 350 ml.

1. What complication occurred in a child?
Answer:
1. Part nephrotic syndrome
FIRST AID brain edema

1. Background. Processes edema and swelling of the brain is one of the most urgent problems of modern intensive care. They accompany a variety of neurosurgical, neurological, surgical and physical illness. Question diagnostic and pathogenetic treatment of edema and swelling of great difficulty for clinicians

2. Specific objectives:
1. Explain the mechanism of brain edema.
2. Recognize the major clinical manifestations of cerebral edema.
3. Interpret supporting research in brain edema (VCHPT, echoencephalography, ultrasound, MRI, CT).
4. To make the algorithm of the physician in cerebral edema.
4.2. The theoretical questions to the studies:
1. Pathogenesis of cerebral edema.
2. Clinical signs of cerebral edema.
3. Characteristics of the Glasgow-Pittsburgh.
4. Diagnosis increase VCHPT and brain edema.
5. Intensive therapy for cerebral edema.

Content themes

Cerebral edema often develops as a result of hypoxia, which occurs at various conditions such as traumatic brain injury, meningoencephalitis, hypercapnia, reducing the osmolarity of plasma fluid and electrolyte disorders, exogenous and endogenous intoxications. This observed loss of consciousness, seizures, vomiting, the presence of which indicates intracranial hypertension.
There edema and swelling of the brain that are stages of the same process: edema - is the accumulation of free fluid in the intercellular space, and swelling - coupled fluid accumulation in cells.
According pathogenesis distinguish vazogennyh, cytotoxic, osmotic, hydrostatic edema. When vazogennyh swelling increases the permeability of blood-brain barrier (BBB) ​​with a yield of plasma in perivascular and extracellular space, accumulate vasoactive substances (prostaglandins, biogenic amines, peptides). Swelling of the brain is observed in TBI, brain tumors, infectious and allergic lesions of the CNS, hemorrhagic stroke. Cytotoxic edema is caused by disorders of cellular metabolism, electrolyte metabolism, increase cell membrane permeability, increased intracellular colloid-osmotic gradient and fluid retention in the middle of the cell during intoxication, hypoxic encephalopathy, postasystolichnomu syndrome, and ischemic stroke. Osmotic swelling of the brain - caused by water intoxication in violation of CNS osmolarity gradient in the plasma of blood - brain parenchyma. Observed in some embodiments the metabolic эntsefalopatiyi (liver, kidney failure, etc.)., Hipoonkotychnyh states, and consequently inadequately conducted eksrakorporalnyh treatments. Hydrostatic brain edema - occurs when fluid everywhere propotivanni ependymu stomachs. It can be observed the syndrome liquor hypertension. In clinical practice, brain swelling, usually has pathogenetically mixed.
Mechanism of cerebral edema: increased permeability of blood-brain barrier, increasing the total pressure, venous outflow from the cranial cavity, reduced osmolarity plasma osmolality increases and decreases hydrostatic pressure of interstitial fluid. Increased fluid content in brain tissue (mainly in glial) cells redistributed into ions of sodium, chlorine, calcium. The number of ATP, increasing nitrogen fraction, ADP, AMP, inorganic phosphorus, oxidized products, developing acidosis. The increase in intracellular calcium leads to the destruction of phospholipid membranes, contributes to the accumulation of fatty acids vysokonasychenyh - substrate prostaglandins. Recent impair brain microcirculation. Arachidonic acid is metabolized to lipoxygenase under the influence of free radicals and leukotrienes. All this contributes to a greater violation of intracranial homeostasis, enhancing the development of edema, swelling of the brain.
Edema may be localized and generalized.
Clinical features of cerebral edema is characterized by general cerebral and focal symptoms.
Zahalnomozkovi symptoms due to increased VCHPT: headache, nausea, vomiting, seizures, impaired consciousness (from lethargy to coma), stagnation in the optic nerve papilla.
It noted the gradual involvement in the pathological process of various brain structures. Lesion of the cerebral cortex is characterized by impaired consciousness, the emergence of generalized clonic seizures. Engaging in the process of subcortical accompanied psychomotor agitation, hyperkinesia, tonic seizures, a characteristic posture decorticate posturing rigidity (curls and leg extension).
Defeat mezentsefalno-hypothalamic area (upper stem and hypothalamus) is accompanied by profound disturbances of consciousness, impaired breathing and circulation. Sudoma a barrel character outside decerebrate rigidity (straightening the arms and legs).
Distribution of edema on lower parts of the brain stem are accompanied by further violations of the respiratory system and cardiovascular system. There have miosis, extension arms with atony feet (destruction of the bridge), mydriasis, absence of pupillary response to light, their central position, diffuse atony, arefleksiya (oblong brain).
The development of focal symptoms associated with displacement of cerebellar hemispheres of the brain and in the future - with herniation and compression of its structures (edema, swelling, head trauma, tumors, hemorrhage).
Intracranial hypertension is characterized by the development of symptoms of irritation of the meninges. Most important is the determination of intracranial perfusion pressure (VCHPT): = AT VCHPT min-1/2 pulse pressure - pressure SMR (mm Hg. Cent.).
Of course, this value is 75-80 mm Hg. century. (9,86-10,65 kPa). When the VCHPT perfusion pressure decreases.
Additional methods of diagnosis of cerebral edema: lumbar puncture, computed tomography, echoencephalography, ultrasound brain and others.
Conducting lumbar puncture is contraindicated in the defeat of an oblong brain, where there bulbar disorders.
To prevent dislocation of the brain at high VCHPT before the puncture is necessary to carry out dehydration. Dislocation of the brain with a temporary effect can be eliminated by introducing endolyumbalnoho 40-60 ml isotonic sodium chloride solution. A more effective method is craniotomy with removal of cerebrospinal fluid from the ventricles.
Biochemical signs of cerebral edema: increased levels of serotonin and histamine, reducing the osmolarity of plasma hypoproteinemia.
When brain swelling noted increased sodium, decreased potassium levels and ATP.
Features of the development of cerebral edema in children. The rapid development of cerebral edema in children is associated with inadequate maturity and high hydrophilic brain tissue, increased permeability of cell membranes, as well as congenital and acquired pathology of CNS allergies. They zahalnomozkovi symptoms may also occur under normal or reduced pressure.

Intensive therapy of cerebral edema.

I. etiopathogenetical: elimination of the causes of disease, treatment of the underlying disease, normalization of gas exchange, stabilization of hemodynamic correction KLS, fluid and electrolyte shifts, metabolic processes dezyntoksykatsiya, anti-allergy therapy; immunocorrection.
II. Local therapy of cerebral edema: normalization of cerebral hemodynamics, including microcirculatory, rheological properties of blood, stabilization of cell membranes, decrease vascular permeability, inactivation of proteolytic enzymes, vasoactive substances, free radicals, normalization of cerebral metabolism, hormone therapy, normalization of intracranial volume and correction of vodnoelektrolitnoho exchange (adequate infusion therapy, dehydration, extracorporeal correction of fluid and electrolyte metabolism), calcium-tubules; hypothermia.
III. Symptomatic: elimination of seizures; correction of temperature homeostasis prophylactic antibiotic therapy, correction of disorders of the internal organs, adequate nutrition, intensive monitoring and care.
Normalization of gas exchange is ensured by maintaining a free airway, oxygen therapy, mechanical ventilation, which is conducted using moderate hyperventilation with PaCO2 4-4,4 kPa (30-33 mm Hg. Cent.). It reduces the blood supply of the brain and improves blood flow in ischemic areas, preventing further growth of brain edema. Continued ventilation on the background vasoconstriction alters brain metabolism and has no effect on the development of edema. Especially appropriate to apply mechanical ventilation in the first 24 hours since the onset of cerebral edema.
The use of HBO is contraindicated due to the risk of oxygen toxicity and increased edema, swelling of the brain.
Hemodynamic stabilization aimed at normalizing CBV, systemic blood pressure, prevent the development of hypo-and hypertension, as well as improving microcirculation (support corpuscular volume at 0,30-0,35 l / l), the rheological properties of blood OCs. While hypertension can be used ganglioplegic (simultaneously reduce the permeability of blood-brain barrier).
1. Normalization of cerebral hemodynamics is provided by improving microcirculation, rheological properties of blood vessel tone. Remember that fast recovery brain circulation is the cause of significant ischemic damage of brain tissue structures. For normalization of cerebral hemodynamics apply: Trental, 5 ml (100 mg) 2% solution, preferably administered intravenously drip. Normalizes z-potential cell increases glycolytic process reduces the loss of potassium by cells, not causes of a "steal syndrome". Children - at 1-3 mg / (kg-day).
Kurantil (dypiridamol) - no effect on hemodynamics without causing hemorrhagic complications syndrome "steal." Inhibits kinin. Apply 2 ml (10 mg) 0.5% solution. Children - by 0.2-0.5 mg / (kg / day). Complamin (Teonikol, Xantinol nikotinat) - 2 ml (300 mg) 15% solution factional or drip. Preparations niacin can impair venous vidtikannya, especially with the rapid introduction. Cavinton - eliminates blood angiospasm, increases the threshold vynoslyvosti to hypoxia, acting as antiagrigant. Not applicable under the threat of hemorrhage. Selectively increases cerebral blood flow. Not be used together with heparin! Assign a dose of 25-30 mg / day for children - by 0.25-0.5 mg / (kg-day) 0.5% solution. Aminophylline - increases the need for oxygen in tissues without affecting the level of oxidative phosphorylation. Causes vasoconstriction of blood vessels of the brain may lead to the emergence of "steal syndrome". When brain edema used with caution. The dose - 6-20 mg / (kg-day), used as a 2.4% solution, children under 1 year, the same solution is injected at the rate of 1 mg / (kg-day) for children aged 2-4 years - 4 mg / (kg-day).
Venous blood vidtikannyu helps position the patient on his back with a raised upper trunk. Turn head to the side, throwing her back increase VTPCH.
Sermion (NICERGOLINE) - in addition to improvement of microcirculation, reduces permeability and capillary fragility. Children are 6-10 mg / (kg-day) 10% solution. A similar action by sulfokamfokayin - 6 - 25 mg / (kg-day). L-lizinu suktsinat 0.1% intravenously 5.0 mL. Low molecular dextran (reopolyglukine) used after stabilization of cellular and vascular membranes with hypervolemia their use is contraindicated. Facilitate the movement of fluid from the intercellular space in the vascular bed, which improves microcirculation. Insecure increased cerebral edema. Children are introduced to 10 ml / (kh-dobu.) in writing speed 0.15 - 0.2 ml / (kg-min). Dopamine is used at the rate of 2 - 5 mg / (kg-min) vasodilation in cerebral vessels.
Drugs that improve cerebral blood flow in the initial stage of swelling (to stabilize cell membranes and vascular) may increase manifestations of cerebral edema.
2. Stabilization of cell membranes and reducing vascular permeability. Dicynone (etamzilat) - 12.5% ​​solution injected 1 ml (125 mg) 3-4 times a day. Children - by 5-25 mg / (. Kg-day). Adrokson - 1 ml of 0.025% solution of 3 - 4 times a day, children - in 0.05-0.1 ml / (kg-day).
3. Inactivation of proteolytic enzymes, vasoactive substances, lipid peroxidation (LPO). Inhibitors of proteolytic enzymes: kontrikal -10 000 IU 2-3 times a day gordoks 100 000 Unit 2 times a day. The course of treatment - 5-7 days may be canceled earlier, after the elimination of the threat of edema.
Remember! Suppress fibrinolysis! Their use is contraindicated in acute respiratory failure.
Aspirin-remember that simultaneously reduces thromboxane A2 and prostacyclin. May increase bleeding.
Antihistamines, drugs (dimedrol, suprastin, tavegil) - 1 ml 3-4 times a day. Children of single dose - 0.1 ml / year of life. Duration of treatment - 5 days.
Antioxidants to reduce lipid peroxidation (tocopherol, ascorbic acid, nicotinamide, and others).
Pyridoxine (vitamin B6). He has the antykininova and antytrypsynova activity, apply 1 ml. Children - by 1.5-3 mg / (kg-day). Similarly operates pyridoxal phosphate (coenzyme vitamin B6).
4. Normalization of cerebral metabolism. Nootropil (piracetam)-increases resistance to hypoxia accelerates the redox processes and utilization of glucose, shows antioxidant effect. Apply a dose of 5 ml (1000 mg) 1-2 times a day. Newborns, by 200-250 mg / (kg-day) in 2 divided doses, for children - 30-50 mg / (kg-day). In patients with convulsive readiness convulsion may occur in the elderly - worsening heart failure. Application is especially effective in the early stages of edema. Nicotinamide - Improves tissue respiration, used for 5-7 mg / (kg-day). β-blockers (Inderal, obzidan, Inderal) - blocking the exit of potassium ions from the cell (anti-hypoxic effect). You can not assign simultaneously with calcium channel blockers (collapse, asystole!). The dose - 1-5 mg (intravenously). Contraindicated in severe right-or left ventricular heart failure, sinus bradycardia, atrioventricular block, bronchial asthma, predisposition to bronchospasm, diabetes with ketoacidosis, pregnancy, disorders of peripheral blood circulation. Antihypoxants: sodium-hydroxybutyrate improves cerebral blood flow, increases oxygen utilization, enzyme activity, antiradical and provides protection antyperekysnyy cells, reduces the level of lactate and pyruvate. Assign the patient with low adaptive-adaptive mechanisms. Detects antihy action. Dose - 50-100 mg / kg. Contraindicated in severe hypokalemia and infants. Seduxen (Sibazon) - single dose of 10-30 mg 3-4 times a day for children - by 0.3-0.5 mg / kg, or 0,8-1,2 mg / (kg-day). Not assigned concurrently with monoamine oxidase inhibitors and derivatives fenotiazydu. Contraindicated in acute liver and kidneys, severe myasthenia gravis.
Seduxen and sodium hydroxybutyrate activating the GABA-energy system of the brain, which reduces swelling.
5. Hormonal drugs primarily affecting the normal brain tissue, preventing cell decompensation and rise of cerebral edema. Not recommended to use in the intracranial hypertension (FK Orkin, L.X. Kuperman, 1985). Effectively operate at perifocal edema caused by the development of tumors. Ineffective in diffusion edema (TBI, hypoxic encephalopathy) their use in appropriate cases vazogennyh edema. Reduce leakage of the liquid part of blood, exert influence cerebroprotective dehydration. Assign: prednisolone-to 1-5 mg / (kg-day); deksazon - 0,1 -0.5 mg / (kg-day). Treatments - 5 days, with no effect within 2 days of treatment should be discontinued. On the mechanism of action similar to nootropics.
6. Normalization of intracranial volume and correction of fluid and electrolyte metabolism: a) the use of an adequate infusion therapy.
Purpose - to maintain normal system pressure. Limiting the amount of fluid during treatment with diuretics may enhance hypoxia and brain swelling due hemokontsentratsiyi, deterioration of microcirculation, oxygenation conditions, between the cell metabolism and blood vessels.
Contraindicated use gemodez, isotonic sodium chloride solution, 5% glucose solution. Avoid sharp increase VCHPT because it can lead to increased edema, swelling of the brain, reducing blood flow, stopping the intracranial circulation and "brain death."
Osmotic diuretics are short, marked dehydration intact plots (syndrome "steal"), repeated hyperhydration syndrome ("rebound"), mainly in the area of ​​edema associated with increased osmolarity. Osmotic diuretics are not used in plasma osmolarity above 320 mOsm / l, intracranial hemorrhage, Nephroses, lack of systemic circulation.
Mannitol-on 0,5-1 g / (kg-day) 10-20%. solution intravenously. Keep in mind the need to prevent the development of dehydration and electrolyte imbalance.
Lasix (furosemide) - at 20-60 mg 1% solution. With repeated administration may gipohloremichesky alkalosis. Children - by 0.5-1.5 mg / kg. Apply with concomitant heart failure.
Drugs that create oncotic gradient between blood and tissues
Albumin - 100-200 ml of 10% solution intravenously, children - to 5-15 ml / (kg-day) in the form of 5 - 10% solution. Fresh frozen plasma - in the same doses.
7. Calcium channel blockers improves microcirculation, normalize hemostatic system, reduce the accumulation of tissue hormones, the brain providing resistance to hypoxia.
Verapamil (izoptyn) - bolus of 5-10 mg (2-4 ml of 0.25% solution), drip-by 0.005 mg / (kg-min). Children - by 0.1-0.2 mg / kg. Enteral: adults - 40-80 mg for children - 1 mg / kg.
Korinfar (nifedipine) - unlike veralamilu without depressing myocardial conductivity, produces weak antiarrhythmic effect, reduces predominantly diastolic pressure. Not recommended for use with low pressure. Assign 10-20 mg three times a day.
H & M at e is n and n - the most effective drug improves overall perfusion in the zone of ischemia of the brain, improves metabolism of neurons in an area that borders the ischemic area.
8. Hypothermia is used for secondary prevention of edema in the background neurovegetative blockade. Reduces the formation of glutamate unprofitable.
Control treatment: definition corpuscular volume, osmolarity of plasma and urine, BCC, electrolytes, VCHPT, dynamics of clinical symptoms.
Prognostic importance of timely the treatment of edema, swelling of the brain.
In the initial stages of swelling of intensive therapy should be aimed at removing the current correction factor with basic functions. Dehydration is not the basis of intensive therapy. When symptomatic cerebral edema intensive care is carried out in full. When decompensation process limited indications for use osmodiuretics and protein drugs (albumin). their purpose may increase the severity of the pathological process.

Materials for self-

Situational task
Task 1. Baby delivered in '11 in the admission department ambulance from city accident. The boy complained of headache, nausea, vomiting, transient impairment of consciousness, when viewed from the skin pale, pupil reaction reduced congestion in the papilla optic nerves, the pulse of the peripheral vessels filiform, stress, heart rate 95 per minute. BP 80/50 mm Hg. century.
1. Your possible diagnosis?
2. Which test should be patient?
3. Is shown holding lumbar puncture?
4. What drugs normalize brain metabolism?
     5. First aid in the treatment of the patient.?
Answers:
1. Swelling of the brain.
2. CT brain
3. Shown in all cases except damage medulla
4. Nootropil, cytochrome C, Panangin, Inderal, nikotinamid.
5. Mechanical ventilation, usually 4 catheters; / in perftoran 3ml/kh; trental 2-3 mg / kg; oksibutyrat sodium 40-120 mg / kg; kaventon 0,25-0,45 mg / kg; L-lizinu suktsinat 0 , 1% 5.0 ml cytochrome C 0.5-0.8 microns / kg deksazon 0.2-0.4 mg / kg per day, according to testimony diuretics

Task 2. The child, 12-years after severe head injury with severe cerebral edema appeared this situation: the child opens his eyes sluggishly, but the look does not register, determined phenomenon tetraparesis, pyramidal signs, dementia, sphincter function is controlled.

1. How is this state out of the coma?
2. What led to the development of this condition?
3. At what scale determine the depth of coma?
4. Which test should be?
5. Assign to treat a patient?
Answers:
1.Opalnyy syndrome.
2.Tryvalyy brain swelling.
3. Scale deep coma Glasgow-Pittsburgh.
4.Yelektroyentsefalohrammu.
5. Preparations for the normalization of cerebral metabolism: nootropic and cardiovascular drugs.

Problem 3. The child, 3 years old, weighing 15 kg, after a severe head injury, according to CT brain determined total cerebral edema.

1. What are the first clinical signs characteristic of this disease?
2. What preparation must first enter?
3. Calculate the dose for this child?
4. What complications may be after the introduction of this drug?
5. Which indicator monitoring required at introduction of this drug?
Answers:
1. Headache, nausea, bradycardia.
2. 20% mannitol.
3. 15g a day.
4. Dehydration and electrolyte shifts.
5. Control of diuresis.
Problem 4. Child 7 years came after road trauma in ICU unconscious. Pupils OD over OS, photo reaction flabby, does not open the eyes to painful stimuli responds not the differential movements.
1. Assessing the level of consciousness by Glasgow?
2. What could be the cause of anisocoria?
3. What method of diagnosis should be first?
4. What indicators should be monitored in this child?
5. What features of cerebral edema in children?
Answers:
1. 18 points
2. Dislocation brain structures.
3. CT brain
4. Arterial and central venous pressure, urine output.
5. The resulting nedostanoyu zrilistyu and high hidrofilnistyu brain tissue.

Problem 5. Child 5 years is being treated on brain edema. In the history of child congenital malformation of the heart. Another doctor prescribed intravenous administration of mannitol. Within 20 minutes after the start of infusion therapy the child's condition worsened: developed cough, increased dyspnea, sputum appeared with a touch of fresh blood.

1. What complication arose in the child and what it involves?
2. Providing emergency and principles for further treatment?
Answers:
1. Pulmonary edema, which is associated with the administration of mannitol in the pathology of heart.
2. Stop administration of mannitol, mechanical ventilation, dehydration therapy adjusted diuretics.