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 (
(
EFP=Hp(47)_Op(25)_ICp(10)=
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
glomerulonephritis, eclampsia.
3. Postrenal: acute renal failure appears due
to complications of
urine outflow (tumours and
calculi of renal pelvis and ureter, prostate,
accidental ligation of the ureters
during operation).
In 70% of the cases acute renal injury appears as a result of
prerenal cause. In stress
conditions (massive blood loss, multiple
injuries) adrenals intensively produce catecholamines: arterioles of
skin, smooth muscles, intestines and kidneys spasm. As you
probably
remember this helps to save the brain and heart
(additional blood for
circulating blood volume), however for the rest
organs this situation,
lasting over 3_4 hours 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_
renal necrosis.
Death of over 75% of nephrons finds its
clinical manifestation in
acute kidneys injury. All the functions of the kidneys– ultrafiltration,
reabsorption, secretion,
bioactive substances production – are
violated.
Stages of acute
kidneys injury: clinic and
treatment
Clinically in 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
less than
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
next possibilities:
1. Hypovolemic shock: profuse bleeding, plasma
loss,
dehydration.
a. restore the circulating blood volume (blood
components
transfusions, colloids and crystalloids infusions,
glucose solutions) –
on time provided correction of circulating blood volume
(and you
will notice it through normalization of blood pressure,
pulse,
haemoconcentration indexes and
especially central venous
pressure) – in most cases means restore of the diuresis.
b. if there is no effect of infusion therapy: 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
infusion pump).
b. use steroids, colloids and crystalloids, steroids
and then –
stimulate the diuresis
(described above).
3. Hemolysis (reactions after blood
transfusions, hemolytic
poisonings, true drowning in sweet water, some
snakebites and insect
bites, myolisis during crash_syndrome):
a. increase the circulating blood volume providing hemodilution
through infusion therapy;
b. increase blood pH infusing 4% solution of sodium
bicarbonate
(however don’t forget to control its level);
c. liquidate spasm of renal arteries;
d. stimulate diuresis.
In case of intense hemolysis, injuries with
massive muscle
disintegration it would be wise to begin preventive hemodyalisis.
4. Renal diseases: normalize hemodynamic indexes, give
spasmolytics, stimulate diuresis and use antihypoxic
treatment.
5. Postrenal reasons of acute kidneys injury
demands immediate
consultation of urologist and decision about operative
liquidation of
urine flow obstruction (insertion of catheters into the
bladder, ureters;
epicystostomy, prostatectomy, lithotomy, etc.). Do not stimulate urine
output with diuretics until the reason of obturation is not removed!!!
Lack of diuretic effects after stimulation states severe organic
injury of nephrons and you should
make a diagnosis 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
renin_angiotensin disorders).
Intensive treatment.
Your therapeutic tactic will differ a lot in comparing with the
previous phase.
1. Fight with overhydration. First of all
medical stuff should
control carefully body weight gain: ideally
correct treatment excludes
increase of the weight. Everyday patient loses
400_500 ml of water
with respiration. Don’t forget to count water loss with
vomiting and
diarrhea. Infusion therapy should not exceed this
total fluid loss and
the only solutions you should use are normal saline and
20_40%
glucose solutions (with insulin).
2. Control and treat electrolyte disorders: prescribe calcium
chloride or calcium gluconate
solutions (40_50 ml of 10% solution
intravenously). Calcium acts as potassium and magnesium
antagonist
and thus lowers their plasma concentrations.
3. Treat metabolic acidosis with 4% sodium bicarbonate solution
(up to 400_500 ml per day with acid_base control tests). Normalization
of blood pH also normalizes potassium level.
4. Catabolism inhibition: to prevent tissues destruction use
anabolic hormones (Nerobol,
Retabolil) which prevent muscle
disintegration and breakdown of the proteins. This helps
to reduce
endogenous water production and toxins production.
For this
purpose we are also using concentrated glucose
solutions.
5. To eliminate the wastes from the body there are different
methods: enterosorbtion
(enterodez, polisorb,
activated charcoal,
etc.), intestinal lavage (cleansing enemas 4_6
times a day),
extracorporeal detoxification methods (hemodyalisis,
plasmapheresis, hemosorbtion),
peritoneal dialysis.
6. Symptomatic treatment: prescribe hypotensive
medicines if
necessary, preparations for cardiac support,
transfuse washed red
blood cells. Prevent infectious complications.
Don’t forget, that in case of acute kidneys injury withdrawal of
many drugs is delayed or interrupted and thus accumulation
effects
are possible!
Hemodialysis is the process of extracorporeal waste
products
removal with the help of “artificial kidney”. The
principle of its work is
quite simple: special pump pushes the blood through the
tubes to the
dialyzer. Dialyzer itself is a system of
capillaries, made of semipermeable
membrane (kuprofan,
cellophane), which are “immersed” into the
dializing solution (something
chemically very close to plasma). When
blood passes through the capillaries dialysis, osmosis 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
over
– 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
adequate.
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
formulas.
Gradually concentrating ability of kidneys is returned and
diuresis is normalized
(specific gravity gets to norm, electrolytes are
reabsorbed).
V. The fifth stage is a stage of recovery. It takes few months or
few years to gain complete recovery and for some patients
everything
will end with a chronic renal failure. In this stage your
task is to
prescribe symptomatic treatment, proper diet and
resort therapy.
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.
Clinical findings:
– skin: jaundice, vascular spiders, “hepatic”
palm, extension of
small superficial face vessels;
– fever;
– hepatic breath odour,
hepatic smell of sweat and urine (this
smell occurs due to transformation of methionine
into methyl
mercaptan);
– digestion disorders (nausea, hiccups, inappetence, smooth red
tongue, abdominal pain, meteorism,
defecation disorders);
– obstructive and diffuse respiration disorders
– hypoxic
hypoxia;
– cardiovascular disorders (arterial
hypotension, tachycardia,
extrasystoles);
– haemorrhagic
syndrome, anemia (due to interruption of
coagulation factors synthesis and bleeding of gastric
or oesophageal
erosions and ulcers);
– frequent additional complications: renal
failure, hepatorenal
syndrome (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).
Intensive
treatment
The basic principle of liver failure treatment is etiologically aimed
therapy: you should treat the reason of the
failure. Two other important
components are prevention and treatment of liver
failure complications
during 10_14 days necessary for the regeneration of the hepatocytes.
Necessary treatment measures:
1. Patient should follow strictly bed regiment in isolated ward.
Medical stuff should follow asepsis and antisepsis rules.
2. Eliminate animal fats and proteins from the patient’s diet to
prevent encephalopathy.
3. Liquidate hepatotoxic factors (hypoxia, hypovolemia,
haemorrhagic syndrome,
intoxication):
– provide oxygen supply (nasal catheter, face mask with the flow
3_4 l/min); sometimes hyperbaric oxygenation and even intestinal
oxygenation (0,2_0,3 ml/kg/min) are possible;
– to increase hepatic blood flow restore the
circulating blood
volume, improve rheological properties of the blood, restore
the
peristalsis. To achieve this you should: infuse
crystalloids and glucose
solutions, spasmolytics,
2 % euphyllin solution (20_30 ml/day). 10%
albumin solution (200_300 ml) and mannitol solution (1 g/kg)
increase oncotic blood
pressure and prevent interstitial oedema of
the liver;
– prevent ulceration of stomach and gastrointestinal bleeding
by prescription of famotidine
or omeprazole (40 mg twice a day);
oesophageal bleedings are
stopped with Blackmore probe;
– if you suspect stagnated blood in the
intestines – remove it,
because otherwise intoxication will get more
intense;
– use only “fresh” blood stabilized with heparin for transfusions.
Prevent and treat intoxication with:
– intestinal lavage
and enemas;
– antibiotics which are not toxic to the liver
(for example
ampicillin 1,0 every 4 hours);
– extracorporeal blood detoxification (plasmapheresis,
hemosorbtion or hemodialysis; usage of artificial liver or artificial
spleen);
– prescribe antagonists of ammonium (40_50 ml of 1% glutamic
acid solution with glucose 3 times a day; 2,0 of alfa_arginine solution
i/v every 8 hours).
4. To stimulate energetic metabolism in hepatocytes
prescribe
concentrated glucose solutions (10_20% solutions, up
to 5g/kg/day).
This will also prevent proteins breakdown and thus wastes
accumulation.
5. To stabilize the membranes of the hepatocytes
prescribe
steroids (10_15 mg/kg of hydrocortisone).
6. To stabilize the energetic exchange and stimulate
transportation of the lipids prescribe choline chloride (10 ml of 10%
solution with 200 ml of glucose solution after
previous atropine
admission, twice a day).
7. Additionally prescribe vitamins (ascorbic acid, B1, B2, B6, K, E,
B12,
folic
and nicotinic acids in doses 2_3 times higher than daily needs),
cardiac glycosides, panangin,
antioxidants (cytochrome c, sodium
gamma_hydroxybutyrate).
8. Symptomatic treatment helps to stabilize homoeostasis if not
to treat failure itself: if necessary use anticonvulsive
medicines,
antipyretics, etc.