Uremic coma is characterized by the following symptoms. Providing emergency care for uremic coma. Stages of development and symptoms

Etiology and pathogenesis of uremic coma

Uremic coma is the final stage of chronic kidney failure (CRN), its extreme stage. The most common causes of CNP: chronic glomerulonephritis to pyelonephritis, polycystic kidney disease, diabetic glomerulosclerosis, amyloidosis. Less commonly, CNP is caused by collagen nephropathies, hypertension, hereditary and endemic nephropathies, tumors of the kidneys and urinary tract, hydronephrosis, and other causes. Despite the variety of etiological factors, the morphological substrate underlying severe CNP is similar. This is a fibroplastic process leading to a decrease in the number of active nephrons, the number of which in the terminal stage of kidney failure drops to 10% or less compared to the norm. In this regard, the end products of metabolism are not completely removed by the kidneys and more and more accumulate in the blood. Currently, more than 200 substances are known that accumulate in increased amounts in various biological fluids of the body with uremia, but it is still not possible to say exactly which of them should be attributed to the "uremic poison". At different times, this role was alternately assigned to urea, uric acid, creatinine, polypeptides, methylguanidine, guanidine succinic acid, and other compounds. Currently, it is believed that "medium" molecules with a molecular weight of 300-1500 Daltons have a toxic effect on the nervous tissue. These include mainly simple and complex peptides, as well as polyanions, nucleotides, and vitamins. "Medium" molecules inhibit the utilization of glucose, hematopoiesis, phagocytic activity of leukocytes. However, it would be wrong to reduce the pathogenesis of uremic intoxication only to the action of "medium" molecules. Of great importance are hypertension, acidotic shifts, electrolyte imbalance, and, apparently, some other factors.

Uremic coma clinic

The development of uremic coma for a long time (several years, rarely months) is preceded by CNP. Initial manifestations of insufficiency are expressed unsharply and are often correctly regarded only retrospectively. Increased fatigue, slight polyuria are noted. Clinical manifestations during this period are due to the nature of the underlying disease. A precomatous state occurs against the background of uremic encephalopathy and damage to other organs and systems (primarily cardiovascular). In the development of uremic encephalopathy, the main role is played by a violation of redox processes in the brain tissue, due to oxygen starvation, a decrease in glucose consumption and an increase in vascular permeability. The rate of development of hyperazotemia is also important (changes in the central nervous system are observed more often and are more pronounced with its rapid development), the level of blood pressure, the frequency of cerebral vascular crises, the severity of acidosis, electrolyte disturbances (of particular importance are the concentration and ratio of individual electrolytes in the cerebrospinal fluid , which do not always coincide with the corresponding indicators in the blood). Symptoms of uremic encephalopathy are nonspecific. Most often, patients complain of headache, blurred vision, increased fatigue and depression, drowsiness (but sleep does not refresh), sometimes alternating with excitement and even euphoria. Sometimes there are psychoses with hallucinations, depression, and later with impaired consciousness of one degree or another (according to the delirious or delirious-amental type). A disorder of consciousness in 15% of cases is preceded or accompanied by their convulsive seizures, which are an indicator of the severity of the condition. The clinical manifestations of seizures are the same as during attacks of renal eclampsia. Just like the latter, they are mainly due to arterial hypertension observed in almost all patients in the late stage of CNP. In addition, an important role is played by metabolic acidosis, hyperhydration (cerebral edema), hyperkalemia, as well as a state of convulsive readiness (genetically determined or resulting from skull injuries, neuroinfection, alcoholism). Changes in the electroencephalogram are nonspecific, similar to those observed in hepatic coma and hyperhydration (decrease in the amplitude of alpha rhythm oscillations, the appearance of pointed and hiccuplike waves, activation of beta waves in the presence of asymmetric theta waves). The severity of these changes does not correlate with the degree of hyperazotemia, but nevertheless, significant EEG changes are observed in the terminal phase of the disease and are a sign of the onset of precoma or coma (especially if they occur suddenly against the background of slowly progressive chronic kidney failure). Apathy and drowsiness, confusion of consciousness gradually increase, giving way at times to excitement with incorrect behavior, and sometimes to hallucinations. In the end, a coma sets in. It can also occur suddenly against the background of moderately severe encephalopathy during pregnancy, surgical interventions, injuries, the addition of intercurrent diseases, the development of circulatory failure, a large loss of potassium during vomiting and diarrhea, a sharp violation of the diet and regimen, exacerbation of the underlying disease (glomerulo- or pyelonephritis, collagen nephropathy, etc.).

In addition to damage to the nervous system, in a precomatous and coma state, there are also manifestations of insufficiency in the function of other organs and systems of the body. In 90% of patients with uremia in the terminal stage, blood pressure rises. Relatively often there are also circulatory failure (mainly left ventricular), pericarditis, Cheyne-Stokes or Kussmaul breathing, anemia, hemorrhagic diathesis, gastritis, enterocolitis (often erosive and even ulcerative).

In recent years, cases of uremic osteopathy and polyneuropathy have become more frequent. There is no complete parallelism between the degree of severity of damage to the nervous system and the concentration of urea, creatinine and residual nitrogen in the blood, but it is still significantly increased in the precomatous and coma state. Often also observed hyperkalemia, hypermagnesemia, hyperphosphatemia, hypocalcemia, hyponatremia, acidosis.

Diagnosis and differential diagnosis uremic coma

If there are indications in the anamnesis of a disease leading to chronic renal failure, and even more so if the patient was observed by a doctor about this insufficiency, then the diagnosis of uremic coma or precoma is not difficult. They occur in cases where there are no indications of kidney disease in the anamnesis (often with primary chronic glomerulonephritis or pyelonephritis, polycystic disease) and renal failure is the first manifestation of the disease. But even in these cases, a precoma or coma is rarely the onset of the disease; it is preceded by other clinical manifestations of renal failure, which progresses relatively slowly. Nevertheless, individual patients with uremia without a "renal history" first come to the doctor in a pre-coma or even in a coma. Then it is necessary to differentiate uremic coma and coma of another etiology. Signs of uremic coma: characteristic skin color, ammonia breath, hypertension, pericarditis, changes in the fundus, changes in the urine. In difficult cases, a biochemical blood test is important (increase in the level of urea, creatinine, residual nitrogen), a decrease in glomerular filtration. True, such shifts are possible in acute renal failure, but in this case there must be appropriate reasons (transfusion of incompatible blood, sepsis, intoxication, etc.), a relatively slow development of azotemia, the absence of oligoanuria, hypertension.

There may also be an idea of ​​a hypochloremic coma that develops with large losses of chlorides (frequent vomiting, profuse diarrhea, diuretic abuse, etc.). But with the latter, vomiting, diarrhea appear long before the development of neurological disorders, changes in the urine are absent or very mild, the amount of chlorides in the blood is sharply reduced, alkalosis is observed.

Establishing the cause that led to the development of uremic coma is important mainly in the case of retention uremia as a result of a violation of the outflow of urine in adenoma or cancer of the bladder, compression of both ureters by a tumor or blockage of their stones. In these cases, the restoration of normal urine flow quickly brings the patient out of the precomatous state. Diagnosis of retention uremia is based on anamnesis data and a thorough analysis of medical records, and in case of their insufficiency, a urological examination is necessary in the urological or intensive care unit (depending on the severity of the patient's condition).

Treatment of uremic coma

Patients who are in a pre-coma or comatose state must be hospitalized in specialized nephrological departments equipped with an “artificial kidney” apparatus for chronic hemodialysis. There, detoxification therapy is carried out: neocompensan or gemodez is intravenously injected 300-400 ml 2-3 times a week, 75-150 ml of 20-40% glucose solution with insulin (at the rate of 5 IU per 20 g of glucose) 2 times a day, and also in the presence of dehydration 500-1000 ml of 5-10% glucose solution subcutaneously. In addition, large doses of lasix are used (from 0.4 to 2 g per day intravenously at a rate of not more than 0.25 g / h). Under their influence, diuresis increases, blood pressure decreases, glomerular filtration increases and urinary excretion of K +, Na +, urea. However, in some patients, there is a refractoriness to the action of derivatives of anthranilic and ethacrynic acids, and other diuretics. The excretory function of the kidneys also increases under the influence of intravenous infusions of isotonic or hypertonic (2.5%) sodium chloride solution, 500 ml intravenously drip. However, with high blood pressure and hyperhydration, the introduction of these solutions is contraindicated. Even with the initial signs of circulatory failure, the introduction of 0.5 ml of a 0.06% solution of cor-glycon or 0.25 ml of a 0.05% solution of strophanthin intravenously is indicated (cardiac glycosides with severe kidney failure are administered at a half dose, the intervals between their administration are lengthened ). Correction of violations of homeostasis is also necessary. With hypokalemia, 100-150 ml of a 1% solution of potassium chloride is administered intravenously, with hypocalcemia - 20-30 ml of a 10% solution of calcium chloride or calcium gluconate 2-4 times a day, with hyperkalemia - intravenously 40% glucose solution and insulin subcutaneously (content potassium must be determined not only in plasma, but also in erythrocytes). With a pronounced acidotic shift, an intravenous infusion of 200-400 ml of a 3% sodium bicarbonate solution or 100-200 ml of a 10% sodium lactate solution is indicated (with severe left ventricular failure, their administration is contraindicated). Antihypertensive drugs are important (4-8 ml of a 1% or 0.5% dibazol solution intramuscularly or intravenously and 1-2 ml of a 0.25% solution of rausedil intramuscularly); in the future, reserpine, clonidine (hemiton), methyldopa (dopegit) are prescribed inside.

Also shown are abundant lavages of the stomach and intestines with a 3-4% solution of sodium bicarbonate. If conservative treatment fails, hemodialysis or peritoneal dialysis is used.

After removal from a coma of patients with retention uremia, transfer. children in the urological department. With uremia of another etiology, treatment with chronic dialysis or peritoneal dialysis is continued (in some cases in preparation for kidney transplantation), with a significant improvement, they are transferred to a low-protein diet (such as the Giova-netty diet).

Prognosis for uremic coma before it was absolutely unfavorable. After the introduction of extrarenal cleansing methods (peritoneal dialysis, hemodialysis, hemosorption), he improved significantly. It is better if these treatments are applied already at the initial clinical manifestations of the pre-coma state, and worse when the coma has already developed. The prognosis is also aggravated by intercurrent diseases, bleeding. Of particular danger are brain hemorrhages, gastrointestinal bleeding, pneumonia. With retention uremia, the prognosis significantly depends on the ability to eliminate the obstruction to the outflow of urine.

Prevention of uremic coma

First of all, timely detection, clinical examination and careful treatment of diseases that most often lead to the development of kidney failure (chronic glomerulonephritis, pyelonephritis, polycystic disease, diabetes, etc.) are necessary. If the insufficiency has already developed, then it is necessary to take all patients to the dispensary as soon as possible and carry out systematic treatment for them. It is necessary to protect them from intercurrent infections, avoid surgical interventions if possible, fight against circulatory failure, bleeding. Women suffering from even the initial degrees of renal failure should not give birth. Planned, systematic conservative treatment of foci of chronic infection (tonsillitis, granulating periadenitis, etc.) is necessary. The issue of operational sanitation is decided in each case individually. It can be made only at initial degrees of a renal failure.

Due to the fact that antibiotics are excreted mainly by the kidneys, their dose decreases as renal failure progresses, and nephrotoxic and ototoxic antibiotics (streptomycin, kanamycin, neomycin, tetracyclines, gentamicin, etc.), as well as sulfonamides, should be avoided. In addition, it is necessary to refrain from the systematic use of opiates, barbiturates, chlorpromazine, magnesium sulfate, both because of the slowing down of their excretion by the kidneys in CNP, and because, against the background of uremic intoxication, the effect of these substances on the central nervous system is more pronounced, and therefore, they may precipitate the onset of uremic coma.

Emergency conditions in the clinic of internal diseases. Gritsyuk A.I., 1985

Certain pathological conditions that can happen to every person require immediate help. The further health of the patient, and in some cases his life, depends on the timely taken rehabilitation measures. This is exactly the case with the development of uremic coma, which is a consequence of chronic renal failure. In this case, the human body is poisoned by various metabolic products, since the affected kidneys simply cannot remove them in full. What measures should be taken in the development of a uremic coma in a patient? And how to recognize the development of this pathological condition?

How does uremic coma manifest itself? Condition symptoms

Before the uremic coma develops in full force, the patient has various manifestations that indicate developing and steadily progressing renal failure. Such symptoms can disturb a person for many months and even years. So, with the development of renal failure, the patient develops profuse diuresis, which becomes especially noticeable at night. However, even with a significant separation of urine, the daily volume of urea, as well as other nitrogenous substances, gradually decreases.

Against the background of such a pathology, there is a significant increase in the content of residual nitrogen in the blood, which leads to the appearance of azotemia. Also, a significant amount of acidic products is retained in the body, provoking acidosis. It is the accumulation of nitrogenous slags, as well as acidosis, that cause the most complex intoxication of the body during the development of uremia. The classic feature of uremic coma is considered to be the slow and gradual progress of all manifestations of the disease. As renal failure increases, the volume of urine excreted decreases in the patient, and oliguria is formed. Even in this case, the specific gravity of the urine does not increase.

As the uremic coma grows, the patient loses the ability to concentrate, he is worried about weakness and fatigue, headaches and a feeling of heaviness in the head. Quite often, pathological processes lead to a deterioration in vision, and over time, there is a decrease in memory, the appearance of drowsiness and apathy. Sometimes the feeling of drowsiness is replaced by active excitement, while the patient does not behave quite adequately, he may be disturbed by hallucinations and confusion.

With the development of uremic coma, the patient experiences hiccups, convulsions, as well as twitching of various muscles of an involuntary nature.

Nitrogenous substances begin to be actively excreted through the digestive tract, which can provoke severe uremic gastritis or colitis. Even in the early stages of the development of uremic coma, the patient has a decrease in appetite, a feeling of dryness in the mouth, he is worried about thirst, nausea, and sometimes vomiting. As the disease progresses, these symptoms are accompanied by diarrhea, in which blood can be seen.

On the mucous membranes of the oral cavity with the development of uremic coma, ulcerative lesions are formed, bleeding from the nose, as well as from the gums, may appear. The air exhaled by the patient has a characteristic smell of ammonia. The skin at the same time is painted in an earthy gray color, becomes dry, itching may appear on it, as well as slight swelling.

What to do when uremic coma begins? Urgent care

If the patient is in a pre-coma or comatose state, he must be immediately hospitalized in the inpatient department, where there is an artificial kidney machine, which makes chronic hemodialysis possible. The patient is given detoxification therapy by injecting hemodez or neocompensated intravenously a couple of times a week. Also, treatment involves the introduction of a glucose solution along with insulin intravenously, and sometimes subcutaneously.

Another drug for emergency care is Lasix.
All of the described compounds help to establish diuresis, lower blood pressure, increase glomerular filtration and ensure the excretion of urea in the urine, as well as potassium and sodium.

To increase the excretory function of the kidneys, an isotonic or hypertonic solution of sodium chloride can also be used, it is also administered by drip intravenously. But it is worth considering that such solutions are not indicated in the presence of hypertension or overhydration.

To correct circulatory failure (even at the initial stage), it is customary to use a solution of corglycon or a solution of strophanin. An important role is also played by the correction of homeostasis disorders.

In the case of hypokalemia, the patient is administered an intravenous solution of potassium chloride, to correct hypocalcemia - a solution of calcium chloride or a solution of calcium gluconate. To eliminate a pronounced acidotic shift, it is customary to use sodium bicarbonate or sodium lactate.

The use of antihypertensive drugs, for example, a solution of dibazol or rausedil, also plays a very important role. Next, the patient is prescribed reserpine, clonidine or methyldopa.

To correct uremic coma, it is also customary to carry out abundant lavages of the intestines and stomach using a sodium bicarbonate solution.
If the conservative treatment does not give the expected effect, the patient undergoes dialysis or peritoneal dialysis.

Methods of urgent correction of uremic coma may differ depending on the causes of the development of this pathology.

Causes of uremic coma

Symptoms of uremic coma

The pathogenesis of uremic coma

What is uremic coma?

Uremic coma (uremia) or urination develops as a result of endogenous (internal) intoxication of the body caused by severe acute or chronic kidney failure.

Causes of uremic coma

In most cases, uremic coma is the result of chronic forms of glomerulonephritis or pyelonephritis. In the body, toxic metabolic products are formed in excess, which sharply reduces the amount of daily urine excreted and coma develops.

Extrarenal reasons for the development of uremic coma include: drug poisoning (sulfanilamide series, salicylates, antibiotics), industrial poisoning (methyl alcohol, dichloroethane, ethylene glycol), shock, intractable diarrhea and vomiting, transfusion of incompatible blood.

In pathological conditions of the body, a violation occurs in the circulatory system of the kidneys, as a result of which oliguria develops (the amount of urine excreted is about 500 ml per day), and then anuria (the amount of urine is up to 100 ml per day). Gradually increases the concentration of urea, creatinine and uric acid, which leads to symptoms of uremia. Due to an imbalance in the acid-base balance, metabolic acidosis develops (a condition in which the body contains too many acidic foods).

Symptoms of uremic coma

The clinical picture of uremic coma develops gradually, slowly. It is characterized by a pronounced asthenic syndrome: apathy, increasing general weakness, increased fatigue, headache, drowsiness during the day and sleep disturbance at night.

Dyspeptic syndrome is manifested by loss of appetite, often to anorexia (refusal to eat). The patient has dryness and a taste of bitterness in the mouth, smells of ammonia from the mouth, increased thirst. Stomatitis, gastritis, enterocolitis often join.

Patients with growing uremic coma have a characteristic appearance - the face looks puffy, the skin is pale, dry to the touch, traces of scratching are visible due to unbearable itching. Sometimes powder-like deposits of uric acid crystals can be observed on the skin. Hematomas and hemorrhages, pastosity (pallor and decreased elasticity of the skin of the face against a background of slight edema), edema in the lumbar region and the region of the lower extremities are visible.

Hemorrhagic syndrome is manifested by uterine, nasal, gastrointestinal bleeding. On the part of the respiratory system, his disorder is observed, the patient is worried about paroxysmal shortness of breath. Blood pressure drops, especially diastolic.

The increase in intoxication leads to severe pathology of the central nervous system. The patient's reaction decreases, he falls into a state of stupor, which ends in a coma. In this case, there may be periods of sudden psychomotor agitation, accompanied by delusions and hallucinations. With an increase in a coma, involuntary twitches of individual muscle groups are acceptable, the pupils narrow, and tendon reflexes increase.

The pathogenesis of uremic coma

The first important pathogenetic and diagnostic sign of the onset of uremic coma is azotemia. In this condition, residual nitrogen, urea and creatinine are always elevated, their indicators determine the severity of renal failure.

Azotemia causes such clinical manifestations as disorders of the digestive system, encephalopathy, pericarditis, anemia, skin symptoms.

The second most important pathogenetic sign is a shift in water and electrolyte balance. In the early stages, there is a violation of the ability of the kidneys to concentrate urine, which is manifested by polyuria. In the terminal stage of renal failure, oliguria develops, then anuria.

The progression of the disease leads to the fact that the kidneys lose the ability to retain sodium and this leads to salt depletion of the body - hyponatremia. Clinically, this is manifested by weakness, a decrease in blood pressure, skin turgor, increased heart rate, thickening of the blood.

In the early polyuric stages of the development of uremia, hypokalemia is observed, which is expressed by a decrease in muscle tone, shortness of breath, and often convulsions.

At the terminal stage, hyperkalemia develops, characterized by a decrease in blood pressure, heart rate, nausea, vomiting, pain in the oral cavity and abdomen. Hypocalcemia and hyperphosphatemia are the causes of paresthesia, seizures, vomiting, bone pain, and osteoporosis.

The third most important link in the development of uremia is a violation of the acid state of the blood and tissue fluid. At the same time, metabolic acidosis develops, accompanied by shortness of breath and hyperventilation.

Etiology and pathogenesis of uremic coma

Uremic coma is the final stage of chronic kidney failure (CRN), its extreme stage. The most common causes of CNP: chronic glomerulonephritis to pyelonephritis, polycystic kidney disease, diabetic glomerulosclerosis, amyloidosis. Less commonly, CNP is caused by collagen nephropathies, hypertension, hereditary and endemic nephropathies, tumors of the kidneys and urinary tract, hydronephrosis, and other causes. Despite the variety of etiological factors, the morphological substrate underlying severe CNP is similar. This is a fibroplastic process leading to a decrease in the number of active nephrons, the number of which in the terminal stage of kidney failure drops to 10% or less compared to the norm. In this regard, the end products of metabolism are not completely removed by the kidneys and more and more accumulate in the blood. Currently, more than 200 substances are known that accumulate in increased amounts in various biological fluids of the body with uremia, but it is still not possible to say exactly which of them should be attributed to the "uremic poison". At different times, this role was alternately assigned to urea, uric acid, creatinine, polypeptides, methylguanidine, guanidine succinic acid, and other compounds. Currently, it is believed that "medium" molecules with a molecular weight of 300-1500 Daltons have a toxic effect on the nervous tissue. These include mainly simple and complex peptides, as well as polyanions, nucleotides, and vitamins. "Medium" molecules inhibit the utilization of glucose, hematopoiesis, phagocytic activity of leukocytes. However, it would be wrong to reduce the pathogenesis of uremic intoxication only to the action of "medium" molecules. Of great importance are hypertension, acidotic shifts, electrolyte imbalance, and, apparently, some other factors.

Uremic coma clinic

The development of uremic coma for a long time (several years, rarely months) is preceded by CNP. Initial manifestations of insufficiency are expressed unsharply and are often correctly regarded only retrospectively. Increased fatigue, slight polyuria are noted. Clinical manifestations during this period are due to the nature of the underlying disease. A precomatous state occurs against the background of uremic encephalopathy and damage to other organs and systems (primarily cardiovascular). In the development of uremic encephalopathy, the main role is played by a violation of redox processes in the brain tissue, due to oxygen starvation, a decrease in glucose consumption and an increase in vascular permeability. The rate of development of hyperazotemia is also important (changes in the central nervous system are observed more often and are more pronounced with its rapid development), the level of blood pressure, the frequency of cerebral vascular crises, the severity of acidosis, electrolyte disturbances (of particular importance are the concentration and ratio of individual electrolytes in the cerebrospinal fluid , which do not always coincide with the corresponding indicators in the blood). Symptoms of uremic encephalopathy are nonspecific. Most often, patients complain of headache, blurred vision, increased fatigue and depression, drowsiness (but sleep does not refresh), sometimes alternating with excitement and even euphoria. Sometimes there are psychoses with hallucinations, depression, and later with impaired consciousness of one degree or another (according to the delirious or delirious-amental type). A disorder of consciousness in 15% of cases is preceded or accompanied by their convulsive seizures, which are an indicator of the severity of the condition. The clinical manifestations of seizures are the same as during attacks of renal eclampsia. Just like the latter, they are mainly due to arterial hypertension observed in almost all patients in the late stage of CNP. In addition, an important role is played by metabolic acidosis, hyperhydration (cerebral edema), hyperkalemia, as well as a state of convulsive readiness (genetically determined or resulting from skull injuries, neuroinfection, alcoholism). Changes in the electroencephalogram are nonspecific, similar to those observed in hepatic coma and hyperhydration (decrease in the amplitude of alpha rhythm oscillations, the appearance of pointed and hiccuplike waves, activation of beta waves in the presence of asymmetric theta waves). The severity of these changes does not correlate with the degree of hyperazotemia, but nevertheless, significant EEG changes are observed in the terminal phase of the disease and are a sign of the onset of precoma or coma (especially if they occur suddenly against the background of slowly progressive chronic kidney failure). Apathy and drowsiness, confusion of consciousness gradually increase, giving way at times to excitement with incorrect behavior, and sometimes to hallucinations. In the end, a coma sets in. It can also occur suddenly against the background of moderately severe encephalopathy during pregnancy, surgical interventions, injuries, the addition of intercurrent diseases, the development of circulatory failure, a large loss of potassium during vomiting and diarrhea, a sharp violation of the diet and regimen, exacerbation of the underlying disease (glomerulo- or pyelonephritis, collagen nephropathy, etc.).

In addition to damage to the nervous system, in a precomatous and coma state, there are also manifestations of insufficiency in the function of other organs and systems of the body. In 90% of patients with uremia in the terminal stage, blood pressure rises. Relatively often there are also circulatory failure (mainly left ventricular), pericarditis, Cheyne-Stokes or Kussmaul breathing, anemia, hemorrhagic diathesis, gastritis, enterocolitis (often erosive and even ulcerative).

In recent years, cases of uremic osteopathy and polyneuropathy have become more frequent. There is no complete parallelism between the degree of severity of damage to the nervous system and the concentration of urea, creatinine and residual nitrogen in the blood, but it is still significantly increased in the precomatous and coma state. Often also observed hyperkalemia, hypermagnesemia, hyperphosphatemia, hypocalcemia, hyponatremia, acidosis.

Diagnosis and differential diagnosis uremic coma

If there are indications in the anamnesis of a disease leading to chronic renal failure, and even more so if the patient was observed by a doctor about this insufficiency, then the diagnosis of uremic coma or precoma is not difficult. They occur in cases where there are no indications of kidney disease in the anamnesis (often with primary chronic glomerulonephritis or pyelonephritis, polycystic disease) and renal failure is the first manifestation of the disease. But even in these cases, a precoma or coma is rarely the onset of the disease; it is preceded by other clinical manifestations of renal failure, which progresses relatively slowly. Nevertheless, individual patients with uremia without a "renal history" first come to the doctor in a pre-coma or even in a coma. Then it is necessary to differentiate uremic coma and coma of another etiology. Signs of uremic coma: characteristic skin color, ammonia breath, hypertension, pericarditis, changes in the fundus, changes in the urine. In difficult cases, a biochemical blood test is important (increase in the level of urea, creatinine, residual nitrogen), a decrease in glomerular filtration. True, such shifts are possible in acute renal failure, but in this case there must be appropriate reasons (transfusion of incompatible blood, sepsis, intoxication, etc.), a relatively slow development of azotemia, the absence of oligoanuria, hypertension.

There may also be an idea of ​​a hypochloremic coma that develops with large losses of chlorides (frequent vomiting, profuse diarrhea, diuretic abuse, etc.). But with the latter, vomiting, diarrhea appear long before the development of neurological disorders, changes in the urine are absent or very mild, the amount of chlorides in the blood is sharply reduced, alkalosis is observed.

Establishing the cause that led to the development of uremic coma is important mainly in the case of retention uremia as a result of a violation of the outflow of urine in adenoma or cancer of the bladder, compression of both ureters by a tumor or blockage of their stones. In these cases, the restoration of normal urine flow quickly brings the patient out of the precomatous state. Diagnosis of retention uremia is based on anamnesis data and a thorough analysis of medical records, and in case of their insufficiency, a urological examination is necessary in the urological or intensive care unit (depending on the severity of the patient's condition).

Treatment of uremic coma

Patients who are in a pre-coma or comatose state must be hospitalized in specialized nephrological departments equipped with an “artificial kidney” apparatus for chronic hemodialysis. There, detoxification therapy is carried out: neocompensan or gemodez is intravenously injected 300-400 ml 2-3 times a week, 75-150 ml of 20-40% glucose solution with insulin (at the rate of 5 IU per 20 g of glucose) 2 times a day, and also in the presence of dehydration 500-1000 ml of 5-10% glucose solution subcutaneously. In addition, large doses of lasix are used (from 0.4 to 2 g per day intravenously at a rate of not more than 0.25 g / h). Under their influence, diuresis increases, blood pressure decreases, glomerular filtration increases and urinary excretion of K +, Na +, urea. However, in some patients, there is a refractoriness to the action of derivatives of anthranilic and ethacrynic acids, and other diuretics. The excretory function of the kidneys also increases under the influence of intravenous infusions of isotonic or hypertonic (2.5%) sodium chloride solution, 500 ml intravenously drip. However, with high blood pressure and hyperhydration, the introduction of these solutions is contraindicated. Even with the initial signs of circulatory failure, the introduction of 0.5 ml of a 0.06% solution of cor-glycon or 0.25 ml of a 0.05% solution of strophanthin intravenously is indicated (cardiac glycosides with severe kidney failure are administered at a half dose, the intervals between their administration are lengthened ). Correction of violations of homeostasis is also necessary. With hypokalemia, 100-150 ml of a 1% solution of potassium chloride is administered intravenously, with hypocalcemia - 20-30 ml of a 10% solution of calcium chloride or calcium gluconate 2-4 times a day, with hyperkalemia - intravenously 40% glucose solution and insulin subcutaneously (content potassium must be determined not only in plasma, but also in erythrocytes). With a pronounced acidotic shift, an intravenous infusion of 200-400 ml of a 3% sodium bicarbonate solution or 100-200 ml of a 10% sodium lactate solution is indicated (with severe left ventricular failure, their administration is contraindicated). Antihypertensive drugs are important (4-8 ml of a 1% or 0.5% dibazol solution intramuscularly or intravenously and 1-2 ml of a 0.25% solution of rausedil intramuscularly); in the future, reserpine, clonidine (hemiton), methyldopa (dopegit) are prescribed inside.

Also shown are abundant lavages of the stomach and intestines with a 3-4% solution of sodium bicarbonate. If conservative treatment fails, hemodialysis or peritoneal dialysis is used.

After removal from a coma of patients with retention uremia, transfer. children in the urological department. With uremia of another etiology, treatment with chronic dialysis or peritoneal dialysis is continued (in some cases in preparation for kidney transplantation), with a significant improvement, they are transferred to a low-protein diet (such as the Giova-netty diet).

Prognosis for uremic coma before it was absolutely unfavorable. After the introduction of extrarenal cleansing methods (peritoneal dialysis, hemodialysis, hemosorption), he improved significantly. It is better if these treatments are applied already at the initial clinical manifestations of the pre-coma state, and worse when the coma has already developed. The prognosis is also aggravated by intercurrent diseases, bleeding. Of particular danger are brain hemorrhages, gastrointestinal bleeding, pneumonia. With retention uremia, the prognosis significantly depends on the ability to eliminate the obstruction to the outflow of urine.

Prevention of uremic coma

First of all, timely detection, clinical examination and careful treatment of diseases that most often lead to the development of kidney failure (chronic glomerulonephritis, pyelonephritis, polycystic disease, diabetes, etc.) are necessary. If the insufficiency has already developed, then it is necessary to take all patients to the dispensary as soon as possible and carry out systematic treatment for them. It is necessary to protect them from intercurrent infections, avoid surgical interventions if possible, fight against circulatory failure, bleeding. Women suffering from even the initial degrees of renal failure should not give birth. Planned, systematic conservative treatment of foci of chronic infection (tonsillitis, granulating periadenitis, etc.) is necessary. The issue of operational sanitation is decided in each case individually. It can be made only at initial degrees of a renal failure.

Due to the fact that antibiotics are excreted mainly by the kidneys, their dose decreases as renal failure progresses, and nephrotoxic and ototoxic antibiotics (streptomycin, kanamycin, neomycin, tetracyclines, gentamicin, etc.), as well as sulfonamides, should be avoided. In addition, it is necessary to refrain from the systematic use of opiates, barbiturates, chlorpromazine, magnesium sulfate, both because of the slowing down of their excretion by the kidneys in CNP, and because, against the background of uremic intoxication, the effect of these substances on the central nervous system is more pronounced, and therefore, they may precipitate the onset of uremic coma.

Emergency conditions in the clinic of internal diseases. Gritsyuk A.I., 1985

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It occurs due to acute or chronic renal failure, which is a complication or stage in the development of almost any kidney disease. According to statistics, uremia ranks 11th among the causes of death among the population after diseases of the cardiovascular system, tumors, diabetes, liver cirrhosis, etc. In descending order of frequency, the causes of uremic coma are: chronic pyelonephritis, chronic glomerulonephritis, diabetic glomerulosclerosis, nephrosclerosis, polycystic and amyloidosis of the kidneys, collagenous nephropathies, intoxications, dielectrolyte nephropathies, metabolic nephropathies, vascular anomalies of the kidneys, etc. Pathogenesis. In a chronic process, uremia develops if 80-90% of the glomeruli are affected. An approximate idea of ​​the size of the lesions is given by the glomerular filtration rate, the level of creatinine in the blood. Along with the death of the structural subunits of the kidney during inflammatory processes, perifocal infiltrations, swelling of the renal parenchyma, and allergic reactions play an undoubted role in the development of renal failure. With a disorder of urodynamics, urostasis, a series of ascending reflexes disrupts blood circulation and lymph circulation in the kidneys, which contributes to a further decrease in their functions. A significant role in the disorders that occur in uremic coma is played by water-electrolyte shifts - dehydration, hypovolemia, dyselectrolytemia, and acid-base balance disorders. In chronic renal failure, turning into a uremic coma, the “contamination” of the blood with protein, acid slags increases, the compensatory-adaptive capabilities of the body are depleted. The content of urea, creatinine, indole products - primarily phenols, methylguanidine, guanidine-succinic acid - increases in the blood. Polypeptides with an average molecular weight (from 300 to 1500), the so-called average molecules, accumulate in the blood. The concentration of calcium increases due to an increase in the production of parathyroid hormone, magnesium ions, various changes in the level of sodium in plasma and tissues occur. Clinical picture. Uremic coma develops gradually, either after an acute renal injury with anuria, or as a result of the evolution of a severe renal disease under the influence of some unfavorable factor. At first, they are worried about sharp weakness, headache, nausea, itching, insomnia, the appearance of a "veil", "fog" before the eyes. Patients become restless, rarely aggressive; in the future - indifference, drowsiness, which turn into sopor and to whom. There are frequent skin, gingival, nasal, uterine, gastrointestinal bleeding (uremic hemorrhagic diathesis). Inspection. The appearance of the patient is noteworthy: a puffy, pale face, most often yellowish-pale due to urochromes accumulating in the skin (ochroderma). The skin is dry, flaky with traces of scratching, arising (sometimes long before the coma) due to itching of the skin. The latter may show urate deposits. Fibrillar twitching of facial muscles, convulsive twitching of the muscles of the extremities and the abdominal wall are observed. The pupils are constricted. Exhaled air with the smell of urine. The vomit has an ammonia odor.


In the clinic of the period preceding the coma and during the coma, gastric, anemic, dyselectrolytemic, neuropsychic syndromes are distinguished, the combination of which determines the characteristics of the disease. Due to the fact that the pressor function of the kidneys is preserved, and the depressive function drops out, the majority of patients have elevated blood pressure numbers. There are other signs of damage to the cardiovascular system, for example, dry uremic pericarditis, myocardial dystrophy (which leads to arterial hypertension, anemia, intoxication), deafness of heart tones, functional murmurs, tachycardia, ECG changes, heart failure. Patients may experience toxic diarrhea, often stomatitis.

Additional research methods. Changes in urine analysis (decrease in specific gravity, the appearance of protein, formed elements) indicate the presence of kidneys, as well as an increase in the content of residual nitrogen, urea, and creatinine in the blood. Signs of dyselectrolytemia are revealed, anemia, leukocytosis appear.

Treatment for uremic coma It is aimed at detoxifying the body, combating emerging acidosis, replacing kidney function. Achieving these goals is especially difficult in cases of slowly developing coma in severe chronic kidney disease. The most effective treatment for this type of coma is hemodialysis and peritoneal dialysis. Both methods have the same indications, but different contraindications. In cases where hemodialysis or peritoneal dialysis is not possible, therapeutic measures should be taken to achieve the goals by other means. For the purpose of detoxification - bloodletting in the amount of 200-400 ml or exchange blood transfusion (4-5 liters) for several days (5-7 times). The introduction of a 5% glucose solution, a 10-20% mannitol solution, a 4% sodium bicarbonate solution in amounts calculated by diuresis; hemodez, gastric lavage with alkaline solutions (for example, soda solution) 2-3 times a day. It is best to wash the stomach with a probe with a 2-3% soda solution in an amount of 4-5 liters. To wash the intestines, siphon enemas with a soda solution in the amount of 6-8 liters and the so-called intestinal lavage are used. Intestinal and gastric lavages help cleanse the blood of toxins. When vomiting, 10 ml of a 10% sodium chloride solution is administered intravenously; 0.5 ml of a 0.1% solution of atropine subcutaneously. When excited, chloral hydrate (50 ml of a 3-5% solution in an enema), phenobarbital, wet wraps are prescribed, with skin itching, washing the skin with cologne, salicylic or camphor alcohol helps. In the case of anemia and a drop in hematocrit below 20%, red blood cell transfusions (200-300 ml) are indicated. Antihypertensive therapy is carried out with the aim of a gradual moderate decrease in blood pressure. To reduce protein catabolism, enhance reparative processes in the kidneys, anabolic steroids are prescribed (nerobol, methandrostenolone 5 mg 1-2 times a day for 15-20 days). An important part of the treatment of precomatous uremia is the appointment of patients with a diet containing a minimum amount of protein, which sharply limits salt intake. The N7a diet developed by the Institute of Nutrition of the USSR Academy of Medical Sciences is recommended. It contains 20 g of protein per day, which is provided by high-grade animal proteins (boiled meat -26.5; egg white), protein-free achloride bread, dishes and side dishes from vegetables, herbs, milk and dairy products, fruits, sugar, vitamin- berry decoctions. The appointment of a low-protein diet in advanced renal failure contributes to the disappearance of uremic symptoms and a decrease in the level of nitrogenous slags (urea, residual nitrogen). However, long-term use of this diet causes patients to feel hungry and lose weight, so as the symptoms of uremia disappear, a less strict diet should be used.

The kidneys play an important role in the body: they remove toxic substances, nitrogenous slags, hydrophilic metabolites, pump and purify the blood, and also regulate the acid-base and water-electrolyte balance. In the event of a violation of the normal functioning of the paired organ, harmful substances and residual waste products begin to accumulate in the blood, which leads to intoxication. The patient develops renal failure, gradually taking on a protracted form, resulting in uremic coma. According to ICD-10, she was assigned the code R39.2 - Extrarenal uremia, R40 - Somnolence, stupor, coma.

Uremic coma is an unconscious state caused by endogenous (internal) intoxication of the body due to severe renal failure. Uremia in Latin means urination. According to the terminology adopted in medicine, it is not considered a disease, but a clinical syndrome that develops against the background of a complete failure of the functions of an organ.

Reasons for the dangerous condition

Uremic coma is the final stage of some protracted diseases. They develop against the background of kidney dysfunction, the causes of which are the following pathologies:

  • pyelonephritis;
  • glomerulonephritis;
  • bilateral urolithiasis;
  • prostate adenoma;
  • diabetes;
  • cystic formations in the kidneys.

Provoke the sudden onset of uremic coma factors that simultaneously lead to the development of acute renal failure and are characterized by a violation of the general and intrarenal circulation:

  • diseases caused by a viral or bacterial infection;
  • acute hemorrhage - vascular bleeding;
  • anaphylactic shock;
  • dehydration caused by vomiting or diarrhea;
  • poisoning with drugs, food, poisons;
  • abuse of alcohol, surrogate products, technical liquids.

Sometimes problems can be caused by congestive processes in the kidneys, which occur due to a violation of the outflow of urine. The membranes of the tubules of the paired organ are destroyed, and urine enters directly into the bloodstream. The condition is accompanied by unbearable sharp pains in the groin area, fever. Blockage of the excretory ducts may be due to the formation of stones or the development of a tumor.

Stages of development and symptoms

The pathogenesis of a severe disease does not depend on age, so both adults and children can suffer. Uremia develops imperceptibly against the background of long-term and sluggish diseases or congenital pathologies. The patient develops profuse diuresis (urination) mainly at night, violations of protein metabolism. In the first case, despite the removal of a large volume of biological fluid, the daily amount of excreted substances decreases - creatinine, indican, urea, amino acids - and the level of residual nitrogen in the blood increases. In the second, there is a delay in acidic metabolic products and acidosis develops.

It's important to know! The intoxication process grows slowly, gradually, over several years. Against the background of the progression of renal failure, the daily amount of urine excreted gradually decreases, and later completely stops, that is, oliguria develops.

A patient with uremic coma may experience the following symptoms:

  • persistent headaches;
  • lethargy drowsiness;
  • nausea, often ending in episodes of vomiting;
  • the appearance of skin itching;
  • partial memory loss;
  • deterioration of vision and hearing;
  • deterioration in concentration;
  • Cheyne-Stokes breathing through the mouth;
  • decrease in performance.

Signs of neuromuscular irritability join the existing ones - hiccups, convulsions, involuntary twitches of individual muscle groups. Uremia in children is many times more severe than in adults. Often they have the following list of symptoms:

  • increased blood pressure;
  • hallucinations;
  • loss of consciousness;
  • change in heart tone;
  • increased bleeding;
  • ulcers and mucous epithelium.

The main criterion for classifying the severity of uremic coma is the level of impaired consciousness. In its course, the disease goes through several stages, each of which is characterized by a certain symptomatology.


During a coma, the scale of the disorder is assessed by criteria such as eye opening, motor and speech reactions. Doctors distinguish three types of it:

  • moderate coma (6-8 points);
  • deep (4-5 b.);
  • terminal (3 points).

The latter is called the transcendental and is considered the most difficult. Against the background of renal failure and the lung that joins it, cerebral edema occurs, the volume of circulating blood decreases, which often causes death.

Consequences of a coma

A serious complication of uremic coma is a problem associated with damage to the nervous system - a change in character, defects in thinking, consciousness, memory. Most clearly, the symptoms appear after the removal of the patient from an unconscious state. In uremic coma, the smell of ammonia comes from the whole body of the patient, and it is felt when air is exhaled. Doctors point to a number of other consequences:

  • osteoporosis;
  • increased bleeding;
  • disturbances of smell, vision and taste.

The most severe complications are cerebrovascular diseases, and the most terrible of all are deep coma and death of the patient.

Comprehensive examination

Confirmation of the diagnosis of uremic coma against the background of long-term renal failure is not difficult. It is much more difficult to identify the disease in the absence of an anamnesis, when the patient is unconscious, and the doctor can rely on clinical manifestations characteristic of uremic intoxication and information from close relatives. In the course of performing diagnostic manipulations, blood tests become the main ones.


Instrumental methods can be used by a doctor if necessary. They include a list of the following procedures:

  • ultrasound examination of the pelvic organs;
  • radiography of the kidneys;
  • electrocardiography;
  • MRI and CT;
  • analysis of cerebrospinal fluid (puncture);
  • conducting mental tests.

It's important to know! After obtaining data from laboratory tests and instrumental studies, differential diagnosis is carried out with diabetic, hepatic and cerebral coma, the latter, unlike the previous two, develops suddenly against the background of a stroke.

Helping the Patient

A patient with a rapidly growing acute renal failure, and especially a person who is in a pre- or coma state, urgent hospitalization is indicated. A difficult situation requires the use of emergency measures in order to prevent the death of the patient. Prior to the arrival of resuscitation doctors, he should be provided with emergency care, and in the future qualified treatment in a hospital.

Urgent measures awaiting doctors

With the development of a coma, the possibilities of providing first aid to loved ones are significantly limited. First of all, in case of inappropriate behavior of the patient, one should try to protect him from bodily harm; during bouts of vomiting, it is recommended to prevent aspiration of the secreted masses. While waiting for the ambulance team, it is advisable to call a nurse and carry out a number of activities:


The patient should be given mineral water with alkali, put an ice compress on his head. With severe nausea and the urge to vomit, you should offer to drink a cold liquid in small sips.

Treatment in a hospital

The evacuation of a patient with acute uremia should be carried out on an ambulance in the supine position on a stretcher, accompanied by a doctor. He enters the intensive care unit, where emergency measures are taken for him: detoxification, restoration of water and electrolyte balance, normalization of blood pressure, symptomatic therapy. In uremic coma, emergency care has the following algorithm.

  1. The degree of impairment of consciousness is assessed according to the Glasgow scale.
  2. The work of the heart and lungs is restored, and in case of a repeated violation, mechanical ventilation, oxygenation, and myocardial massage are used.
  3. Emergency diagnostic procedures are carried out.
  4. Indicators such as blood pressure, pulse rate, and breathing are continuously monitored.
  5. The gastrointestinal tract is washed with a 2% solution of sodium bicarbonate, and saline laxatives are prescribed.

The most effective is the process of extrarenal blood purification - hemodialysis. From the moment of admission to the medical facility, the medical staff is advised to treat the patient as potentially serious.

Conservative therapy

Conservative treatment of uremic coma should begin at an earlier prehospital stage. The acute form of renal coma lends itself to rapid and effective therapy, the fight against protracted pathology takes much more time.

The following tactic is considered optimal.

  1. Correction of the drinking regime - an increase in the daily volume by 500 ml to compensate for the lack of fluid.
  2. Salt-free diet - cooking meals with the addition of a limited amount of table salt.
  3. Reducing the formation of nitrogenous compounds - limiting protein intake to 40 g per day. Adequate calorie content of food should be maintained at the same time.
  4. Prevention of the development of anuria or oliguria - reducing the amount of fluid consumed, the exclusion of salt from the diet, taking "Furosemide".
  5. Antihypertensive therapy - taking diuretic drugs, primarily Corinfar.

Treatment of infectious complications, including pneumonia, diseases of the urogenital area, a course of antibiotic therapy with drugs of the penicillin group, macrolides is considered mandatory. Reception of means without nephrotoxic action is shown.

Surgery

In the case of the development of irreversible changes in the renal tissue, radical measures are resorted to - kidney transplantation. In modern medicine, its transplantation from a human donor is used. The main indication is the complete loss of functionality of the paired organ and the terminal stage of chronic renal failure, when the patient is at risk of death. In anticipation of transplantation (if indicated), the patient is on regular hemodialysis. The operation may not be for everyone. There is no clear list of contraindications, each clinic presents its own list. However, the following pathologies are considered absolute:

  • cross-immunological reaction with donor lymphocytes;
  • HIV infection;
  • chronic form of hepatitis B and C.

Relative contraindications (that is, after their elimination, transplantation is considered possible) include:

  • oncological processes - 2 years after radical treatment;
  • tuberculosis - after a year of observation of the condition with adequate therapy .;
  • decompensated extrarenal pathologies;
  • mental disorders.

A refusal can be received by a patient who has no contraindications, but who at the same time does not observe discipline at the preparatory stage, does not follow the recommendations of the attending physician, and leads a hectic lifestyle.

Rehabilitation after uremic coma

Recovery from uremic coma should be aimed at eliminating the underlying cause of the disease and its prevention. As methods to help avoid the development of uremia, experts indicate:

  • regular medical examination;
  • prevention or timely treatment of infectious diseases;
  • exclusion of injuries and poisoning, as well as the occurrence of other provoking factors.

In the case of pregnancy planning, it is necessary to undergo a thorough diagnosis for a young couple, as well as family members of both partners to identify renal pathology.

Prognosis after treatment

Until recently, the prognosis for patients suffering from uremia was unfavorable, but in recent years, statistical indicators have improved significantly. Today, subject to the timely application for qualified medical assistance, the chances of a complete recovery and return to a normal rhythm of life have appeared in 65-95% of patients. Exceptions are cases with particularly severe forms of damage to the urinary system and the inability to carry out extrarenal blood purification, which inevitably leads to death.

It's important to know! It became possible to provide high-quality assistance to a patient at any stage of uremic coma, even terminal, thanks to the use of an artificial kidney apparatus. Regular hemodialysis can increase life expectancy by 20 years or more.

Conclusion

To date, acute uremia is considered curable, a serious condition lends itself well to correction, but only in the case of timely adequate therapy and the use of hemodialysis. Full recovery of the patient is possible after a year, less often - six months. If, during an acute attack, emergency care turned out to be late or was not carried out at all, then almost all cases end in death.