Methods of Examination 4 страница. Renal arterial hypertension involves specific changes in the fundus oculi (renal retinopathy)

Renal arterial hypertension involves specific changes in the fundus oculi (renal retinopathy). But these changes, attending kidney diseases, are often due not only to the spasms of arteries and arterioles of the retina but also, in a certain measure, to the upset permeability of retinal capillaries; they also occur during final stages of chronic diseases of the kidneys that end with nephrosclerosis, uraemic toxicosis, and haemorrhagic syndrome.

Certain stenosis of arteries and arterioles of the retina, tortuosity of fine veins of the yellow spot, and flatness of the veins at their crossing with the arteries, with small ampoule-like dilatation before the crossing (Hann-Salus symptom), are observed during the first period (first degree). The pa­tient does not complain of deranged vision; the changes are only transient and functional. Further, due to a continuing spasm and hyalinosis of the arteriolar walls, their lumen narrows, larger arteries become stenosed and tortuous, the veins are compressed by the crossing arteries, and their ampoule-like dilatations before the crossing point become more pronounc­ed (second degree). In the final stage, the arteries and arterioles are highly tortuous and markedly affected by spasms; they resemble silver wires; small veins of the retina are consolidated and sclerosed, they bend at the point of crossing with the arteries and are impressed into the retina to simulate a rupture (the third degree). Greyish-white and yellow foci of oedema and retinal dystrophy and haemorrhages are revealed; the papilla of the optic nerve is oedematous. Foci of dystrophy radiating in the area of the yellow spot often have a stellar shape. Vision is deranged due to dystrophic changes in the fundus oculi and haemorrhages.

It should be noted that the fundus oculi is a very convenient site where fine vessels can be visualized, as well as changes occurring in them and the surrounding tissues (in the retina) during the course of the disease. The study of the fundus oculi is therefore very informative for the diagnosis and prognosis of a renal disease. In certain cases, the patient consults first the ophthalmologist for his impaired vision, because renal diseases can for a long time develop without vivid symptoms. The specific changes in the fundus oculi help in such cases suggest renal pathology (which is later con­firmed by the appropriate studies).

Finally, disorders in cerebral circulation with paralysis, deranged sen-

sitivity, dysfunction of the pelvic organs, and also myocardial infarction can develop as a result of arterial hypertension and atherosclerosis.

It follows therefore that in certain kidney diseases, the renal hyperten­sion syndrome can be of primary significance in the clinical picture of the disease and can be decisive for its course and outcome.

Renal Eclampsia

Eclampsia (Gk ek lampein to flash) usually develops in acute diffuse glomerulonephritis, but can also arise in aggravated chronic glomerulonephritis and nephropathy of pregnancy. The pathogenesis of eclampsia is largely underlain by increased intracranial pressure, oedema of the cerebral tissue and cerebral angiospasm. Eclampsia in all these con­ditions usually arises in pronounced oedema and increased arterial pressure. Attacks of the disease are provoked by salted food and excess li­quid.

The first signs of approaching eclampsia are often unusual somnolence and flaccidity. These are followed by severe headache, vomiting, tem­porary blindness (amaurosis), aphasia, transient paralysis, mental confu­sion, and a rapid rise in the arterial pressure. Convulsions develop unex­pectedly, sometimes after uttering a cry, or after a noisy deep inhalation. The convulsions are first strong tonic spasms, which are followed (in 0.5-1.5 minutes) by strong clonic contractions. Less frequently only twitching of some muscles is observed. The face becomes cyanotic, the neck veins swell, the eyes turn aside or roll up, the tongue is bitten, and foam emerges from the mouth. The pupils are dilated and do not respond to light; the eyeballs are firm. The pulse is tense, slow, the arterial pressure increases. The body temperature rises in frequent attacks. Involuntary defaecation and urination often occur.

Attacks of renal eclampsia usually last for a few minutes, rarely for longer time. Eclampsia occurs in some cases as a series of two or three at­tacks which follow one another. The patient then calms down to stupor, deep sopor or coma; consciousness is then regained. After recovery from the state of stupor the patient sometimes remains in amaurosis (blindness of the central origin) and aphasia (mutism).

This is the classical picture of an eclampsia attack. But it should be-remembered that attacks of eclampsia may also be atypical; they may occur without loss of conciousness or occur in an obliterated form, as a transient aphasia, amaurosis, and mild muscular twitching.

Renal eclampsia should be differentiated from convulsions of other origin. Convulsions in eclampsia are the same as in epilepsy (a congenital or post-traumatic nervous disease). But oedema or other signs of renal in-

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sufficiency are absent in epilepsy; attacks of convulsions usually occur in the course of many years. Convulsions develop also in uraemic coma, but the patient has a typical anamnesis in this case (chronic renal insufficiency), signs of uraemic toxicosis, slow (in the course of several days) development of the convulsive state; the character of convulsions is different as well: convulsions develop as slight fibrillary twitchings.

Treatment. An attack of renal eclampsia can be removed immediately by a suboccipital or cerebrospinal puncture with extraction of a small por­tion of the cerebrospinal fluid: the intracranial pressure decreases and the patient regains consciousness. The extraordinary efficacy of cerebrospinal puncture proves the importance of increased intracranial pressure for the pathogenesis of attacks of renal eclampsia. Phlebotomy and intravenous injection of magnesium sulphate (10 ml of a 25 per cent solution) remove attacks of eclampsia, effectively decrease the arterial pressure and lessen cerebral oedema.

Renal Failure

Renal failure is toxicosis of the body caused by renal dysfunction (self-poisoning). Uraemia is a severe form of renal failure. Renal failure and uraemia occur in acute and chronic cases. Acute uraemia develops in poisoning with nephrotoxic substances (compounds of mercury and lead, carbon tetrachloride, barbiturates, etc.), in transfusion of incompatible blood, profuse haemolysis, and shock. Chronic uraemia develops in the final stage of many chronic renal diseases, such as chronic glomerulonephritis, pyelonephritis, amyloidosis, affections of the renal vessels, tumours of the kidneys, etc.

Pathogenesis. It consists in profound homeostatic disorders. It has been established that products of protein decomposition are accumulated in the blood of patients with uraemia. These are nitrogenous slags, such as urea, uric acid, creatinine, and other guanidines. The content of indican, phenol and other aromatic substances that are formed in the intestine and pass into the blood through the intestinal wall (normally, these substances are •eliminated from the blood by the kidneys) increases. Various com­pounds of sulphur, phosphorus, magnesium, and other substances are ac­cumulated; the ionic equilibrium is upset. Acidosis develops as a result of the accumulation of acid products and disordered production by the kidneys of ammonia that neutralizes the acids. Uraemia is attended by a grave affection of the liver and metabolic disorders.

Acute renal failure and acute uraemia develop due mainly to shock and the accompanying circulatory disorder (mostly in the kidneys). Anoxia develops to cause dystrophic changes in the renal glomeruli and tubules. In

other cases, when acute renal failure is due to poisoning or a grave infec­tious disease, its pathogenesis is largely determined by the direct action of poisons and toxins on the renal parenchyma. In both cases glomerular filtration is deranged, diuresis decreases and oliguria develops; in severe cases anuria may occur. Salts of potassium, sodium, phosphorus, nitrous products and some other substances are retained in the body.

Acute renal failure rapidly develops and the patient's condition becomes grave: vomiting, mental confusion, deranged respiration and upset heart activity are observed. The glomeruli are affected by ischaemia to raise the arterial pressure; oedema develops in anuria. The patient may die unless anuria and azotaemia are removed during the first few days. If the course of the disease is benign, diuresis increases but the concentrating capacity of the kidneys remains impaired for some time; the renal function gradually normalizes and the patient recovers.

Clinical picture. Acute renal failure varies slightly, depending on the character of the main disease. In many cases it proceeds with some general symptoms which make a syndrome. Four stages of acute renal failure are distinguished: (1) initial stage lasting from several hours to 6-7 days; its clinical picture is characterized by the main symptoms of the disease (traumatic or transfusion shock, severe infectious disease, poisoning, etc.); (2) oligoanuric stage characterized by changes in diuresis (to complete anuria), uraemic toxicosis, and water-electrolyte disorders. Proteinuria, cylindruria, and erythrocyturia are revealed on examination. The oligoanuric stage can end with death of the patient or his recovery. In the latter case, diuresis suddenly or gradually increases (the third or polyuric stage). The specific gravity of the urine is low, the concentration of residual products of protein metabolism in the blood decreases, water-electrolyte balance is restored and the pathological changes in the urine disappear. The fourth stage, recovery, begins with normalization of diuresis; it lasts from 3 to 12 months.

Development of chronic renal failure is determined by the progressive affection of the kidney parenchyma. The latent period of chronic renal failure, when renal dysfunction has no clinical symptoms and can only be revealed by special laboratory methods, and the manifested period, characterized by the marked clinical picture of uraemia, are distinguished.

The latent period can only be revealed by special tests carried out for concentrating capacity of the kidneys and cold food and by the Zimnitsky test. The patient's urine is usually of low specific gravity (below 1.017). Variations in specific gravity are only insignificant (isohyposthenuria). The clearance tests reveal disordered reabsorption in the renal tubules and in glomerular filtration. Mild renal dysfunction can be revealed by radioisotope nephrography. It is believed that the first signs of renal failure

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in patients with chronic renal diseases only appear when the functioning parenchyma diminishes to at least one fourth of its normal size.

Progressive renal failure is attended by changes in the circadian varia­tions in urination: isuria or nycturia are observed. The concentration and dilution tests reveal significant disorders in the concentrating capacity of the kidneys, pronounced isohyposthenuria (the specific gravity of all urine specimens varies from 1.009 to 1.011, i.e approaches the specific gravity of plasma ultrafiltrate, the " primary" urine). More pronounced disorders in reabsorption and glomerular filtration are determined by the clearance tests and nephrography. Concentration of nitrogenous substances in the blood gradually increases. Residual nitrogen increases several times (its normal content is 14.2-28.5 mmol/1 or 20-40 mg/100 ml). Laboratory studies reveal increased concentration in the blood of various products of protein decomposition: urea (3.23-6.46 mmol/1 in norm and 10-15 and more times higher in renal failure), creatinine (0.088-0.176 mmol/1 in norm and 1-1.3 mmol/1 in renal failure), indican (0.68-5.44 ^mol/1 in norm). It should be noted that the increased blood indican content is often the first and the most reliable sign of chronic renal failure, because its blood content does not depend on the protein concentration of food and because it is not accumulated in tissues.

Moderately increased concentration of products of nitrogenous decom­position in the blood {azotaemia) may have no effect on the subjective condition of the patient for a certain period of time. But later some exter­nal changes become manifest and they can be used for the diagnosis of uraemia. Certain symptoms of uraemia depend on partial compensation of renal failure by a more active involvement of the skin, mucosa, and the digestive glands in the excretory processes. Decomposition of the urea (ex­creted by the mucosa of the air ways and the mouth) to ammonia by the bacteria accounts for the specific uraemic breath. In serious cases, the uraemic breath can be felt by the physician as he approaches the patient's bed. It is believed that the uraemic breath can be felt when the concentra­tion of residual nitrogen in the blood exceeds 70 mmol/1 (about 100 mg/100 ml).

The nitrogenous substances, and in the first instance urea, are liberated by the gastric mucosa and decomposed to form ammonia salts. These salts irritate the mucosa of the stomach and the intestine to stimulate nausea, vomiting (uraemic gastritis), and diarrhoea (uraemic colitis). Irritation of the respiratory mucosa causes laryngitis, tracheitis, and bronchitis. Severe stomatogingivitis develops. The mucosa becomes affected by ulcers and necrosis. Urea crystals (as a white powder) can sometimes be seen on the patient's skin. This is especially noticeable at the orifices of the sweat glands (at the base of hairs). Strong itching develops and the patient scrat-

ches his skin. Poisons accumulated in the blood are also liberated by the serous membranes. Uraemic pericarditis is especially characteristic. It can be revealed by auscultating the heart using a stethoscope: the specific coarse pericardial friction can be heard. This friction appears in the ter­minal period and is a sign of approaching death.

Memory and sleep become deranged due to general poisoning; weakness, dull headache, somnolence, apathy and deranged vision are characteristic. Examination of the fundus oculi reveals narrowed arteries and dilated veins, oedema of the papilla of the optic nerve, and whitish local foci (retinopathy). Development of retinopathy is explained by trophic disturbances due to the vascular spasm of the fundus oculi vessels and uraemic toxicosis which intensifies these changes. The pupils are usual­ly narrowed.

Metabolic disorders are pronounced: the patient develops cachexia; the liver and bone marrow functions are affected by dystrophy; toxic uraemic anaemia develops which is usually attended by leucocytosis and throm-bocytoperiia. The tendency to haemorrhages develops due to a decreased blood platelet count, disorders in the blood coagulating system and in­creased capillary permeability (as a result of toxicosis). Haemorrhages of the gastro-intestinal tract, urinary tract, uterus, and the nose may develop. Skin haemorrhages also occur. The body temperature slightly decreases.

Later, toxicosis increases, the patient's consciousness becomes dimm­ed, and uraemic coma develops. Periods of stupor alternate with periods of excitation, hallucinations, and noisy slow breathing with very deep inspira­tions (Kussmaul's breathing); respiration with alternating periods of hyperpnoea and apnoea (Cheyne-Stokes respiration) occurs less frequent­ly. At the terminal stage the patient is in a deep coma; muscular twitchings occur at times and the patient dies.

There is no universally accepted classification of chronic renal failure at the present time. Three stages are usually differentiated: (1) the initial stage with insignificantly increased residual nitrogen and creatinine and moderately decreased glomerular filtration; (2) pronounced stages (IIA and IIB) with marked azotaemia and electrolyte disorders and (3) terminal stage with a pronounced clinical picture of uraemia.

Main principles of treatment. Patients with acute renal failure should
be immediately taken to hospital. Treatment should be begun as early as
possible and aimed at eliminating the main aetiological factors (removal of
nephrotoxic substances or their detoxication, giving large doses of plasma
or blood substitutes for hypovolaemic shock). The electrolyte equilibrium
should be corrected simultaneously. Mannitol or furocemid should be
given intravenously in the initial functional stage of acute renal failure to
restore diuresis. Haemodialysis (artificial kidney) or peritoneal dialysis are
necessary in grave cases..

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The protein content of the diet is controlled in patients with chronic renal failure. Therapeutic action on the aetiological factor and pathogenic mechanisms should be attempted (antibacterial therapy in pyelonephritis immunodepressants in chronic glomerulonephritis, etc.). The water-electrolyte equilibrium and acid-base balance are corrected simultaneously. The necessary symptomatic therapy with hypotensive, cardiovascular and other preparations should be carried out. In severe cases, permanent chronic haemodialysis is carried out or the kidneys are transplanted to pro­long the patient's life.