Intensive care of acute kidney and hepatic insufficiency
Acute renal failure
Kidneys are the pair organs located in the retroperitoneum (at
the level of 12_th rib in the loin region). Their main function is
elimination of the metabolic wastes from the organism. They are
supplied with blood by paired renal arteries, which are direct arterial
branches of abdominal aorta.
Nephron is the basic functional unit of the kidneys. Its structure
is quite complicated: it consists of renal corpuscle (Bowman_
Shumlanski’s capsule and glomerulus), proximal convoluted tubule,
loop of Henle, distal convoluted tubule and direct tubule.
Kidneys are exclusively “hard_working” organ. Their total weigh
is hardly 0,4% of the total body weight, however they receive 25 % of
cardiac output. 10% of total inhaled oxygen are used for their
metabolic needs. During the day nearly
are ultrafiltrated out of the blood. Ultrafiltration is possible only
when effective filtration pressure is not less than
defined as a difference between hydrostatic (
So when hydrostatic pressure (mean arterial pressure) is
decreasing or when intracapsular pressure is reaching critical values
filtration stops and renal failure appears.
In tubules water, electrolytes and glucose are reabsorbed and
metabolic wastes are secreted to the urine. Eventually during one
day only 1 % of primary urine is evacuated from the organism in the
form of secondary urine with high concentration of toxic substances.
Kidneys participate in haematopoiesis, regulation of fluid
balance, electrolytes metabolism and acid_base balance.
Kidneys are also organs of secretion: their parenchyma produces
rennin – substance very important for vascular tone regulation.
Etiology and pathogenesis of acute renal failure
(acute kidneys injury)
Acute kidneys injury is a syndrome appearing due to sudden and
progressive affection of nephrones, which causes violation of renal
function and induces life_threatening homoeostasis disorders.
The reasons of acute kidney injury are divided into 3 gorups:
1. Prerenal: pathological conditions, which lower renal blood flow,
such as hypovolemia, hypotension, thrombosis, renal artery embolism,
renal artery spasm, haemolysis, myolysis (muscle desintegration). Thus
the prerenal failure can be connected with the massive blood loss, shock
(traumatic, anaphylactic, cardiac), dehydration (burns, pancreatitis,
peritonitis, vomiting, diarrhoea), crush_syndrome, transfusion of
incompatible blood, acute respiratory failure.
2. Intrinsic: the primary damage is caused to the renal
parenchyma by exogenous toxins (alcohol surrogates, acetic acid,
ethylene glycol, heavy metal salts), nephrotoxic antibiotics
(aminoglycosides), bacterial toxins (in case of sepsis), acute
3. Postrenal: acute renal failure appears due to complications of
urine outflow (tumours and calculi of renal pelvis and ureter, prostate,
accidental ligation of the ureters during operation).
In 70% of the cases acute renal injury appears as a result of
prerenal cause. In stress conditions (massive blood loss, multiple
injuries) adrenals intensively produce catecholamines: arterioles of
skin, smooth muscles, intestines and kidneys spasm. As you probably
remember this helps to save the brain and heart (additional blood for
circulating blood volume), however for the rest organs this situation,
lasting over 3_4 hours means ischemia and even necrosis.
Another mechanism for acute renal failure is connected with the
acute vascular insufficiency (collapse, endotoxicosis). Hydrostatic
pressure decreases and thus filtration of the blood lowers.
The mechanism of this pathological process is next:
hypoperfusion_renal ischemia_hypoxia_coagulation of blood in
glomerular vessels_termination of plasma filtration_affection of
tubules membranes– compression of the nephrons and capillaries_
Death of over 75% of nephrons finds its clinical manifestation in
acute kidneys injury. All the functions of the kidneys– ultrafiltration,
reabsorption, secretion, bioactive substances production – are
Stages of acute kidneys injury: clinic and
Clinically in case of acute kidneys injury we differentiate 5 stages:
I. First stage (initial) is the stage of shock: depends on the initial
aggressive agent and duration of its influence. It can last several hours
or several days (2_3). Clinic also depends on the causing factor,
however first of all you should observe carefully the haemodynamics
and urine output, because correct evaluation of patient’s condition
and proper treatment may prevent the development of next stages.
Warring symptoms are:
– arterial hypotension (systolic blood pressure
Hg if it remains during few hours);
– decrease of urine output;
– hyposthenuria (low specific gravity– less than 1006_1008)
Intensive treatment depends on the primary disease. So you have
1. Hypovolemic shock: profuse bleeding, plasma loss,
a. restore the circulating blood volume (blood components
transfusions, colloids and crystalloids infusions, glucose solutions) –
on time provided correction of circulating blood volume (and you
will notice it through normalization of blood pressure, pulse,
haemoconcentration indexes and especially central venous
pressure) – in most cases means restore of the diuresis.
b. if there is no effect of infusion therapy: liquidate renal arteries
spasm and restore microcirculation _ give β_adrenoceptor antagonists
(droperydol, aminazin, ganglionic blockers, epidural anesthetics);
stimulate diuresis with 30% mannitol solution 1 g/kg i/v with the
speed 80_100 drops per minute (with 40% glucose solution), 1%
furosemid solution (beginning with 2_4 ml every 7_10 minutes and
up to 40_50 ml); use additionally spasmolytics (10 ml of 2% euphillin
solution i/v with saline). This “triple shot” combined with infusions
can liquidate the functional renal failure.
2. Acute vascular insufficiency: anaphylaxis, toxic collapse,
orthostatic collapse caused by overdose of ganglionic agents or
β_adrenoceptor antagonists; “warm phase” of bacterial shock;
reflectory cardiogenic shock.
a. stabilize vascular tone and perfusion pressure with
adrenomimetics (epinephrine, dopamine, mezaton i/v, best of all with
b. use steroids, colloids and crystalloids, steroids and then –
stimulate the diuresis (described above).
3. Hemolysis (reactions after blood transfusions, hemolytic
poisonings, true drowning in sweet water, some snakebites and insect
bites, myolisis during crash_syndrome):
a. increase the circulating blood volume providing hemodilution
through infusion therapy;
b. increase blood pH infusing 4% solution of sodium bicarbonate
(however don’t forget to control its level);
c. liquidate spasm of renal arteries;
d. stimulate diuresis.
In case of intense hemolysis, injuries with massive muscle
disintegration it would be wise to begin preventive hemodyalisis.
4. Renal diseases: normalize hemodynamic indexes, give
spasmolytics, stimulate diuresis and use antihypoxic treatment.
5. Postrenal reasons of acute kidneys injury demands immediate
consultation of urologist and decision about operative liquidation of
urine flow obstruction (insertion of catheters into the bladder, ureters;
epicystostomy, prostatectomy, lithotomy, etc.). Do not stimulate urine
output with diuretics until the reason of obturation is not removed!!!
Lack of diuretic effects after stimulation states severe organic
injury of nephrons and you should make a diagnosis of acute renal
failure, stage of oligoanuria.
II. Second stage– oligoanuria– lasts from several days to 3 weeks
(duration depends on the degree of the damage and regeneration
ability of the nephrons). It can manifest as oliguria (urine output less
than 500 ml/day) or anuria (urine output less than 50 ml/day).
The severity of this stage is determined with its symptoms:
1. Overhydration: quite often it is caused by iatrogenic reasons –
doctors try to “overfill” patient with the water to stimulate diuresis
(outdated and dangerous conception!) or simply calculate the daily
fluid balance in a wrong way (too “positive” balance).In addition this
phase is characterized by intensive catabolism (tissues destruction)
and thus excessive endogenous water production (up to 1500 ml/
day). Clinical findings: increase of the body weight, circulating blood
volume, blood pressure, central venous pressure, peripheral oedema,
possibly pulmonary oedema.
2. Electrolytic disorders: hyperkalemia, hypermagnesemia,
hypocalcemia. Clinical findings: depression, somnolence, hyporeflexia,
respiratory and cardiac disorders.
3. Metabolic acidosis is caused by accumulation of hydrogen ions
due to disorders of their renal secretion. Clinical findings: noisy rapid
deep breathing (compensatory Kussmaul breathing), vomiting,
evident haemodynamic disorders.
4. Uraemic intoxication. Clinical findings: consciousness
disorders (up to coma), ammonia breath odour, uraemic polyserositis
(pleuritis, pericarditis), ulceration of oesophageal mucous membrane
and gastric mucous membrane, diarrhoea.
5. Disorders of synthetic renal function. Clinical findings: anaemia
due to erythropoietin deficiency and hypertension (connected with
Your therapeutic tactic will differ a lot in comparing with the
1. Fight with overhydration. First of all medical stuff should
control carefully body weight gain: ideally correct treatment excludes
increase of the weight. Everyday patient loses 400_500 ml of water
with respiration. Don’t forget to count water loss with vomiting and
diarrhea. Infusion therapy should not exceed this total fluid loss and
the only solutions you should use are normal saline and 20_40%
glucose solutions (with insulin).
2. Control and treat electrolyte disorders: prescribe calcium
chloride or calcium gluconate solutions (40_50 ml of 10% solution
intravenously). Calcium acts as potassium and magnesium antagonist
and thus lowers their plasma concentrations.
3. Treat metabolic acidosis with 4% sodium bicarbonate solution
(up to 400_500 ml per day with acid_base control tests). Normalization
of blood pH also normalizes potassium level.
4. Catabolism inhibition: to prevent tissues destruction use
anabolic hormones (Nerobol, Retabolil) which prevent muscle
disintegration and breakdown of the proteins. This helps to reduce
endogenous water production and toxins production. For this
purpose we are also using concentrated glucose solutions.
5. To eliminate the wastes from the body there are different
methods: enterosorbtion (enterodez, polisorb, activated charcoal,
etc.), intestinal lavage (cleansing enemas 4_6 times a day),
extracorporeal detoxification methods (hemodyalisis,
plasmapheresis, hemosorbtion), peritoneal dialysis.
6. Symptomatic treatment: prescribe hypotensive medicines if
necessary, preparations for cardiac support, transfuse washed red
blood cells. Prevent infectious complications.
Don’t forget, that in case of acute kidneys injury withdrawal of
many drugs is delayed or interrupted and thus accumulation effects
Hemodialysis is the process of extracorporeal waste products
removal with the help of “artificial kidney”. The principle of its work is
quite simple: special pump pushes the blood through the tubes to the
dialyzer. Dialyzer itself is a system of capillaries, made of semipermeable
membrane (kuprofan, cellophane), which are “immersed” into the
dializing solution (something chemically very close to plasma). When
blood passes through the capillaries dialysis, osmosis and ultrafiltration
take place. During this process toxic wastes (creatinine, urea, uric acid,
phosphates, potassium and hydrogen ions) and excessive water move
to the dializing solution. Simultaneously ions of sodium and calcium
move from the dializing solution into the blood.
According to the method of blood taking and blood return
dialysis is conducted through arterial_venous access or venous_
venous access. Aseptic conditions are obligatory; anticoagulants are
used in most cases (heparin solution). Average blood speed of 200_
250 ml/minute determines duration of dialysis up to 4_5 hours.
Absolute indications to haemodialysis are:
– overhydration (CVP
– hyperkalaemia (potassium more than 7 mmol/l);
– creatinine more than 0,3 mmol/l;
– decompensated metabolic acidosis (pH<7,2);
– daily growth of urea > 5 mmol/l, urea level over 35 mmol/l.
Contraindications to haemodialysis:
– unstable haemodynamics
(blood pressure less than
– haemorrhagic syndrome;
– decompensated cardiac and respiratory insufficiencies;
– CNS damages (stroke, intracranial haematoma).
III. Third stage is a stage of diuretic function restoring. It begins
when the daily urine output becomes more than 500 ml and lasts
for 3_5 days. Due to regeneration of the glomeruli blood filtration
is gradually restored. Tubules epithelium regenerates a bit slower
and thus water reabsorption is still inadequate. Diuresis growth
every day and at the end of this phase reaches 1500_2000 ml per
day. However urine has low specific gravity and contains large
amount of red blood cells and protein. Hyperkalaemia and uraemic
intoxication are still dangerous, because wastes elimination is not
So the intensive treatment is quite similar to the previous stage.
You can change the volume of infusions (but again – control the
daily balance of fluid). When daily urine output will reach physiologic
point of 2_3 liters next stage starts.
IV. Forth stage is a diuretic stage (polyuria). It lasts up to 2
weeks. Daily diuresis increase is 800_1000 ml and daily urine output
reaches 7_9 liters. Biochemical blood tests get to the norm (urea,
creatinine). Due to excessive diuresis dehydration and electrolyte
imbalance develop: potassium and magnesium ions are lost in large
amounts and this can bring life_threatening complications.
Intensive treatment hass changed: now your task is to restore
the circulating blood volume and lost electrolytes reserves.
Correction is made according to the laboratory tests and special
Gradually concentrating ability of kidneys is returned and
diuresis is normalized (specific gravity gets to norm, electrolytes are
V. The fifth stage is a stage of recovery. It takes few months or
few years to gain complete recovery and for some patients everything
will end with a chronic renal failure. In this stage your task is to
prescribe symptomatic treatment, proper diet and resort therapy.
Acute liver failure
Liver is the largest internal organ, unpaired triangular gland
located in the right upper quadrant of the abdominal cavity, below
the diaphragm. It is extremely important for the organism because
of the variety of activities it performs. Liver is a digestive gland
(produces and excretes bile necessary for lipids consumption), a
detoxification centre (microsomal oxidation allows detoxification
of exogenous and endogenous toxic substances) and a synthetic
center, where proteins, lipids and carbohydrates are metabolized.
Liver is also an organ of haematopoiesis and a blood reservoir.
Additionally it helps to control acid_base balance.
To provide its metabolic needs with the oxygen organism gives
nearly 25% of total consumed oxygen; in case of severe intoxication
this number growth up to 40% of the total oxygen. Blood flow of the
liver is for 20% provided by hepatic arteries and for 80% by the portal
vein. Thus the blood liver receives is poorly oxygenated and any
hypoxic condition will bring oxygenation disorders first of all to the
tissues of the liver. This evolutionary resulted in unique regeneration
abilities of the liver: death of 70% of cells will end up with a failure;
however after a certain adaptation period hepatic tissues will restore
their quantity and quality.
7.2. Acute liver failure: etiology and pathogenesis
Acute liver failure is a state of hepatic cells dysfunction, caused
by unknown earlier liver disease, resulting in general intoxication,
coagulation violations, neurological and mental disorders. Its
etiology is usually connected with: viral hepatitis (hepatitis B virus,
hepatitis A virus), poisonings (mushrooms, dichlorethane,
phosphorus, carbon tetrachloride, arsenic), eclampsia, burn disease,
anaesthetic gas, antibiotics, sulfanilamides, massive bacterial
pneumonia, cirrhosis, hepatic tumours and metastases.
Advanced liver failure manifests in coma. Hepatic coma is divided
into endogenous (“destructive”, hepatocellular) and exogenous
(“shunt”, porto_caval). Toxic damage of 70% of liver cells will cause
endogenous coma. In case of liver cirrhosis high portal pressure
antagonizes portal blood flow and thus most of the blood moves to
the caval venous system and is not detoxified – exogenous coma
appears. Clinically we usually observe mixed comas.
Central nervous system in case of liver failure is affected in various
ways. Ammonia encephalopathy appears because of violations of uric acid
synthesis (it is made from ammonia and without this process ammonia
concentration increases several times). Food reach with proteins stimulates
ammonia encephalopathy onset, as well as gastrointestinal bleedings,
hypnotic medicines and opiates, alcohol, surgeries, infections and metabolic
alkalosis. In the CNS tissues false mediators like octopamine, amino acids
and their toxic metabolites are accumulated. On the background of
hypoproteinemia interstitial edema appears and this brings respiratory
hypoxia of tissues. At the same time violated synthesis of enzymes,
disordered metabolism of carbohydrates and lipids, metabolic alkalosis
with hypokalaemia just advance the encephalopathy.
Clinical findings in case of liver failure
Liver failure has several forms:
1. Excretory form (disorders are mostly connected with bile
production, jaundice is the main characteristic).
2. Vascular form (clinically portal hypertension is the most noticeable).
3. Hepatocellular form (most clinical sings are caused by disorders
of synthetic metabolism in liver cells).
According to the duration of the process we define acute and
chronic liver failure, according to the compensation level–
compensated, subcompensated and decompensated failure.
Central nervous system is damaged gradually: it begins with
precoma and progresses into moderate and deep coma.
– skin: jaundice, vascular spiders, “hepatic” palm, extension of
small superficial face vessels;
– hepatic breath odour, hepatic smell of sweat and urine (this
smell occurs due to transformation of methionine into methyl
– digestion disorders (nausea, hiccups, inappetence, smooth red
tongue, abdominal pain, meteorism, defecation disorders);
– obstructive and diffuse respiration disorders – hypoxic
– cardiovascular disorders (arterial hypotension, tachycardia,
– haemorrhagic syndrome, anemia (due to interruption of
coagulation factors synthesis and bleeding of gastric or oesophageal
erosions and ulcers);
– frequent additional complications: renal failure, hepatorenal
syndrome (prognostically very dangerous).
If liver failure progresses CNS damage deepens and you can
clinically observe: weakness, headache, sluggishness, apathy, inversion
of sleep and awakening. Disorientation develops gradually, there is
possibility of excitement periods and cramps. You can also find
overactive tendon reflexes, foot clonus, Babinski’s sign. One of the most
significant symptoms is flapping: trepidation of limbs and face, especially
of hands in prone position (arms extended). In case of deepest coma you
will see dilated pupils, eyeballs are fixed, tendon reflexes are absent.
Progressive and quick decrease of liver size is a prognostically
bad sign. However when the disease is chronic and fibrous changes
took place this symptom is not noticed (liver stays enlarged).
The basic principle of liver failure treatment is etiologically aimed
therapy: you should treat the reason of the failure. Two other important
components are prevention and treatment of liver failure complications
during 10_14 days necessary for the regeneration of the hepatocytes.
Necessary treatment measures:
1. Patient should follow strictly bed regiment in isolated ward.
Medical stuff should follow asepsis and antisepsis rules.
2. Eliminate animal fats and proteins from the patient’s diet to
3. Liquidate hepatotoxic factors (hypoxia, hypovolemia,
haemorrhagic syndrome, intoxication):
– provide oxygen supply (nasal catheter, face mask with the flow
3_4 l/min); sometimes hyperbaric oxygenation and even intestinal
oxygenation (0,2_0,3 ml/kg/min) are possible;
– to increase hepatic blood flow restore the circulating blood
volume, improve rheological properties of the blood, restore the
peristalsis. To achieve this you should: infuse crystalloids and glucose
solutions, spasmolytics, 2 % euphyllin solution (20_30 ml/day). 10%
albumin solution (200_300 ml) and mannitol solution (1 g/kg)
increase oncotic blood pressure and prevent interstitial oedema of
– prevent ulceration of stomach and gastrointestinal bleeding
by prescription of famotidine or omeprazole (40 mg twice a day);
oesophageal bleedings are stopped with Blackmore probe;
– if you suspect stagnated blood in the intestines – remove it,
because otherwise intoxication will get more intense;
– use only “fresh” blood stabilized with heparin for transfusions.
Prevent and treat intoxication with:
– intestinal lavage and enemas;
– antibiotics which are not toxic to the liver (for example
ampicillin 1,0 every 4 hours);
– extracorporeal blood detoxification (plasmapheresis,
hemosorbtion or hemodialysis; usage of artificial liver or artificial
– prescribe antagonists of ammonium (40_50 ml of 1% glutamic
acid solution with glucose 3 times a day; 2,0 of alfa_arginine solution
i/v every 8 hours).
4. To stimulate energetic metabolism in hepatocytes prescribe
concentrated glucose solutions (10_20% solutions, up to 5g/kg/day).
This will also prevent proteins breakdown and thus wastes
5. To stabilize the membranes of the hepatocytes prescribe
steroids (10_15 mg/kg of hydrocortisone).
6. To stabilize the energetic exchange and stimulate
transportation of the lipids prescribe choline chloride (10 ml of 10%
solution with 200 ml of glucose solution after previous atropine
admission, twice a day).
7. Additionally prescribe vitamins (ascorbic acid, B1, B2, B6, K, E,
B12, folic and nicotinic acids in doses 2_3 times higher than daily needs),
cardiac glycosides, panangin, antioxidants (cytochrome c, sodium
8. Symptomatic treatment helps to stabilize homoeostasis if not
to treat failure itself: if necessary use anticonvulsive medicines,