Bleeding and blood loss.
Methods temporary control of bleeding.
Methods final control of bleeding.
Haemorrhage, or bleeding, is the escape of blood from
the blood vessels into the tissues and cavities of human body or outside, as
the result of an injury or defect in the permeability of the blood vessel wall.
During every damage the bleeding is arised.
The hemorrhage is one of the main reasons of death of persons with trauma. The bleeding, its consequences, methods of a first aid and treatment are studied from the moment of origin of medicine. Despite of it, some questions of this problem till are completely unsolved.
The surgeons are to placing a high emphasis to a problem of a bleeding. One of the basic parameters of qualification of the surgeon’s skill is reduce a loss of blood during operation and to stop a bleeding.
About
a bleeding speak, when the blood actively acts from a vessel (vessels) in an
environment, hollow organ or cavities of an organism.
In some cases the blood to ooze into the suurrounded tissues as a result of bleeding. This process is named extravasate.
In other cases when the poured
out blood causes stratification of tissues, separation of organs and as a
result the dimension cavity arised, which is filled with a blood is formed, -
we speak about a hematoma
(fig.1). The
further development of a hematoma may lead to the following results. These are resorption, suppuration or
the organization of a hematoma. The
hematoma which is communicating with a lumen of the injured arteria, is called
aneurismal (pulsative) hematoma. Clinically
it is shown by definition of a pulsation of a hematoma during palpation and
presence of systolic hum during auscultation.
Classification. There are some classifications
of bleeding.
I. Anatomical classification
(according to kind of bleeding vessel):
·
Arterial hemorrhage;
·
Venous hemorrhage;
·
Capillary hemorrhage;
·
Parenchymatous hemorrhage.
II. According to mechanism of beginning:
·
Mechanical failure, vessel rupture (haemorrhagia per
rhexin);
·
Arrosive hemorrhage (haemorrhagia per diabrosin). This
types of bleeding takes place during suppurative melting of wessel wall;
·
Diapedetic hemorrhage (haemorrhagia per diapedesin);
·
The violation of chemical composition of blood. The
hemophilia, scarlet fever, sepsis, scurvy and others are causing bleeding
sometimes. Toxins or beriberi to produce defect in the permeability of the
vascular walls and caused of hemorrhage;
·
Increased of arterial and venous blood pressure. The
diseases, such as essential hypertension, atherosclerosis sometimes coursed of
an injury of the vascular wall and bleeding (stroke, hemorrhoidal bleeding,
etc.);
·
Violation of fibrillation (haemophilia, Werlgof’s disease,
cholemic hemorrhage in patients with jaundice).
III. According to environment the bleeding
divided into the two main kinds. There are:
·
External bleeding;
·
Internal bleeding.
The hemorrhage during damaging of skin or visible
mucous membrane is named external. When blood accumulates in the enclosed space
of the body or in the cavity or in the hollow organ – this is internal
bleeding. Internal hemorrage divided into the explicit and occult (without
clinical symptoms). Moreover, it can
be occult, when diagnosed only by means of specific methods of investigation.
In arterial external bleeding blood of bright red
ciliur effuses by pulsative spurt. Such haemorrhage quickly results in acute
anemia. The following symptoms characterize an acute anemia: persisting paleness,
trembling and small pulse, progressing decrease of blood pressure, dizziness,
nausea, vomiting and syncope.
External venous bleeding is characterized by slow
effusion of dark blood.
Injury of large veins of neck is dangerous due to
a possibility of development of air embolism of cerebral vessels and cardiac
pressure in these veins during ingalation.
General symptoms are the same for all types of bleeding, including inner bleeding in various cavities. They are observed in heavy loss of blood and consist of appearance of acute anemia (paleness, dizziness, syncope, trembling small pulse, progressing decrease of blood pressure).
The local symptoms are various.
In internal bleeding, blood effused into closed
cavity, may compress a vitally important organ (brain, heart, lung, etc.),
violate its function and become dangerous for the patient’s life.
Bleeding in serous cavities (pleural, abdominal)
during internal haemorrhage the especial place is occupied. They stop
independently rarely and are noted massiveness of a hemorrhage. It is caused by
that the blood in a serous cavity loses ability to coagulation. Walls of these
cavities don’t obstruct mechanically to the escape of blood through injured
vessel. Moreover, owing to negative pressure in a pleural cavity it is formed
suction effect. As a result of falling out a fibrin from a blood coagulation is
violate. A fibrin settles on a serous cover. Thus process of a thrombogenesis
is impairing.
At bleedings in empty space of a gastrointestinal
tract the blood in a stomach changes the color. In ample quantity of its accumulation a vomiting, like
“ground coffe” (hematemesis),
is originated. Further or at a
bleeding from underlaying departments of a gastrointestinal tract it is
observed weak tarry stool in large quantity
(melena). This is example of explicit bleeding.
Occult bleeding – this is hemorrhage without any clinical symptoms. For
example, there is bleeding from ulcer of stomach or duodenum. This type of
heamorrhage doesn’t have clinical symptoms. Such bleeding is possible to reveal only by laboratory method. This is
research of occult blood in feces. Continued long time concealed hemorrhages which are not revealed, may result in
development of an anemia.
Some kinds of internal bleeding have specific
name:
·
Haemobilia – haemorrhage from diliary ducts;
·
Haematuria - haemorrhage from kidneys and urinary system;
·
Haemoperitoneum - haemorrhage in abdominal cavity;
·
Haemothorax - haemorrhage in pleural cavity;
·
Haemopericardium - haemorrhage in pericardial cavity;
·
Haemartrosis – haemorrhage in joint cavity;
·
Metrorrhagia – uterine bleeding;
·
Proctorrhagia – rectal bleeding;
·
Hemorrhagic insult – cerebral hemorrhage.
IV. According to time of beginning all bleeding are: primary and secondary.
A beginning of primary bleeding is concemed with
direct damaging of vessel during trauma. Straight off onset symptoms or durig
first hours after injuring be developed.
The secondary bleedings are early (usually from some hours to 4-5 days after damaging) and late.
There are two main reasons of early secondary
bleeding development:
1. Slide of ligature off
damaging vessel, which was imposition during operation;
2. Washing-out the clot
from the injured vessel. This complication we have in connection with increased
of blood pressure, blood flow acceleration or through reduction of spastic
vessel contraction, which to occur during acute blood loss.
Late secondary or arrosive hemorrhage concemed with vessel wall destruction. This is
result of development of wound infected process. This case is one of very
complicated, because all vessel wall change in this region and hemorrhage
replace in every moment is possible.
V. According to clinical course – all bleedings are divided into acute and chronic.
During acute haemorrhage to bleed occurs at short
time period.
During chronic haemorrhage to bleed is gradually,
a little at a time. Sometimes during some days narrow or periodic discharge of
blood is observable. In cases of stomach ulcer, duodenum ulcer, malignant
tumors, uterine fibromyoma, hemorrhoids the chronic haemorrhare is observe.
VI. According to degree of severity.
Estimation of blood loss severity is very
important, because it determined of character of blood supply disturbance in
sick organism and finally, danger of bleeding for patient’s life.
According V.I.Struchkov and E.W.Lutzevich
there four levels of blood loss.
·
I level – easy degree –
blood loss is even to 10 – 12% of blood circulating volume (500 – 700 ml).
Haemorrhage is causing little changes to hemodynamic. The general condition of
patient is satisfactory. Pulse is slightly quickened, arterial pressure is
normal (standart). Blood hemoglobin is rised above 100 g/l (10 g %). During
capillaroscopy: background is rosy, 3 – 4 capillary loops with quick gomogenous
bloodstream are determined.
·
II level – middle degree -
blood loss is even to 15 – 20 % of blood circulating volume (1000 – 1400 ml).
Apparent bleeding is distinguished. The general condition is medium-scale
difficalty. Limpness, dizziness, hyperhidrosis, syncope are observed. Coverlet
is pale. Respiration is accelerated. Reflexes are decrease. Single vomitting or
melena may be observed. Pulse become noticeably more rapid (90 – 100 per min.).
Arterial pressure is decreased to 90 mm Hg. Leucocytosis, deviation of the
differential count to the left are determined. Hematocrit is 0,38 – 0,32,
hemoglobin is 80 – 100 g/l (8 – 10 g %). Quantity of urination is decreased.
·
III level – heavy degree –
blood loss is 20 – 30 % of blood circulating volume (1500 – 2000 ml). The
general condition of patient is bad (grave condition). Paleness of skin, cold
sweat is observed. Rapid vomiting and melena are determined. The bleeding is
accompanied by syncope. Visible mucous membranes are colourless. The patient
yawns, feels thirst. Pulse is rapid and thready. Arterial pressure is decreased
to 60 mm Hg. Hematocrit is 0,30 – 0,32, hemoglobin is 50 – 80 g/l (5 – 8 g %).
Oliguria is observed.
·
IV level – massive blood loss
– loss of blood is more then 30 % of blood circulating volume (more than 2000
ml). Plentiful bleeding with prolonged loss of consciousness may be observed.
The general condition of patient is very grave, preagony. Pulse and arterial
pressure are not fixed. Hematocrit is 0,23 and lower, hemoglobin is 50 g/l and
lower. Anuria is observed.
Clinical picture of
haemorrhage.
The clinic is characterized by local and general appearances.
The
local symptoms depend on kind of bleeding (external or internal), and in what
body or a cavity the blood is flowing into.
The general symptoms are some already. The massive hemorrhage is characterized by paleness of a skin, cold sweat, breathlessness, fast thready pulse and drop of arterial and venous pressure, sometimes syncope. The patient has dizziness, flashing before eyes, dryness in a mouth, thirst, nausea, weakness, irritability, an excessive sweating and decrease of urination. In a blood there are fall in erythrocytes, haemoglobin, hematocrit content and relative density.However, owing to the fact to development compensatory - adaptive mechanisms at the first hours after a hemorrhage hematological parameters may stay kept within the normal limits. It sometimes will disorient the doctor.
Sometimes the bleeding from the big arterias may stop on its own. These can occue the influence of series of circumstances:
1. Drop of arterial pressure, as
consequence of a bleeding which continues;
2. The general vasospasm, as
compensatory parameter;
3. Reduction of the injured
vessel, especially after the complete cutting it;
4. Inverting inside internal and average walls of a vessel in a place of its break.
The compensatory - adaptive mechanisms during acute blood loss are:
·
Spasm of
veins;
·
Interstitial fluid inflow;
·
Tachycardia;
·
Oliguria;
·
Hyperventilation;
·
Peripheral arteriolespasm;
·
Sympaticoadrenal system’ activation;
·
Activation of fibrillation system and
haemopoiesis stimulation.
Features of a major bleed?
·
Tachypnoea
·
Tachycardia >100 bpm.
·
Hypotension SBP <100mmHg supine or postural
drop at any stage. Relate BP to the patient’s normal e.g. hypertensive.
·
Clammy, cold and peripherally shutdown.
·
Conscious level reduced/confusion.
·
History of syncope.
Is the patient at Significant Risk of Death?
·
Hypotensive after initial resuscitation.
·
Variceal bleed likely.
·
Obvious signs of chronic liver disease or
deranged clotting indicative of liver disease.
·
Continuing melaena, haematemesis, or rebleed.
·
Existing co-morbidity e.g. IHD, renal failure,
disseminated malignancy.
·
Age >60 years.
Complicating factors
·
Co-morbid disease e.g. cardiovascular,
respiratory, renal, malignancy.
·
Rate limiting drugs prevent compensatory
tachycardia e.g. ß-blockers, verapamil.
·
Vasodilators prevent compensatory
vasoconstriction, e.g. ACE inhibitors.
TREATMENT
Laboratory investigations. Checking for levels of the erythrocytes, haemoglobin and hematocrit should be done on admission and repeated afterwards. In severe haemorrhage, the results of the investigations mentioned may not serve as objective indicators of the degree of bleeding in the first few hours, since autohaemodilution occurs with time, reaching its maximum within 1,5 – 2 days.
It is haematocrit and blood specific gravity which can be relied upon in judging about the interrelationship between the cellular components of blood and plasma.
The blood specific gravity of as much as 1,057 – 1,054, haemoglobin 65 – 62 g/l, haematocrit 44 – 40 suggest blood loss as high as 500 ml, while those of 1,049 – 1,044, haemoglobin 53 – 38 g/l and haematocrit 30 – 23, respectively, mean that the amount of the blood loss is above 1000 ml.
A progressive fall in venous blood pressure suggests that the heart is not receiving enough blood due to a reduction in blood circulating volume. It is measured either in the superior or inferior vena cava. This is performed with a catheter passing through the median cubital or saphenous vein. The most factual method is whereby the amount of blood loss is checked by calculating the deficit in blood circulating volume and its components (i.e. circulating plasma volume, volume of cellular blood components, etc.). The method consists in the introduction of specific indicators (Evans’ blue, radioisotopes, etc.) into the vascular system. The concentration of the diluted indicator in the blood helps determine the plasma volume; using the standard table and the haematocrit value allows for the calculation of blood circulating volume and globular volume. The normal values of blood circulating volume and its components are found from the standart table based on the patoent’s body weight and sex. The difference between the normal and the actual values is used to estimate the deficit in blood circulating volume, circulating plasma volume and the globular volume, i.e. the amount of blood lost.
Special diagnostic methods. If internal bleeding is suspected, diagnostic puncture should be performed (thoracocentesis during haemothorax, laparocenthesis during haemoperitoneum, arthrocentesis during haemartrosis and puncture of the posterior vaginal fornix during ruptured ectopic gestation or ovarian cyst). If indicated, X-ray, ultrasound scanning and computerised tomography can also be used. Endoscopic methods include gastroscopy, rectoscopy, cystoscopy and arthroscopy.
It will be noted that clinical symptoms and syndromes as well as the laboratory findings are used to evaluate the severity of blood loss.
Complications of bleeding
The hemorrhagic shock may arise at an acute hemorrhage and volume of a circulating blood reduction. The hemorrhagic shock is one kind of a hypovolemic shock. The clinical picture of it may occur since a blood loss 20 - 30 % of volume of a circulating blood. But much depends on an initial condition of the patient.
Allocate three stages of a hemorrhagic shock (G.A.Rjabov and co-authors, 1983).
1 stage - is the compensated
convertible shock (a set of symptoms of small emission). It is characterized by
such volume of a hemorrhage which is well filled with compensatory - adaptive
abilities of the patient’s organism.
2 stage – is irreversible
(decompensated) convertible shock. It is characterized by deeper circulatory
disturbances. The spastic stricture of arterioles may not support the central
hemodynamics any more and normal amount of arterial pressure. Further at
accumulation of metabolites in tissues to occur paresis of capillary channel.
Decentralization of bloodstream develops.
3 stage - is irreversible shock. It is characterized by long (more than 12 hours) an uncontrollable hypotonia, an inefficiency of transfusion therapy and development of multiple organ failure.
Among other complications it is possible to name a false aneurysm (arterial and arteriovenous), an air embolism.
The basic disorders which develop during a bleeding:
1.
A hypovolemic shock caused by decrease of a circulating blood volume;
2.
Renal insufficiency caused by decrease of a filtration and a hypoxia of kidneys
parenchyma;
3.
Hepatic insufficiency as a result of decrease of hepatic bloodstream and
hypoxia;
4.
A myocardium anoxia which results in cardiac infarction;
5.
A hypoxia of a brain which results in an edematization of a brain;
6. By products of protein hydrolysis of blood intoxication, this was poured out in an intestine or other cavities.
Mallory–Weiss
Syndrome
Introduction
Mallory and Weiss first described gastroesophageal
tears causing gastrointestinal bleeding in 15 alcoholic patients in 1929. Since
this time, longitudinal mucosal lacerations, associated with forceful retching,
has become a well-known cause of upper gastrointestinal bleeding. The
prevalence of Mallory–Weiss Syndrome is reported to be approximately 5% of
patients suffering acute upper gastrointestinal bleeding, but may be higher.
The presence of Mallory–Weiss tears without acute bleeding is difficult to quantify
and their clinical significance is debatable.
Etiology and
Pathogenesis
The
pathogenesis of Mallory–Weiss tears is not completely understood, but it is
thought that they are most likely caused by a sudden increase in
intra-abdominal pressure. This is most likely secondary to forceful emesis, but
can be due to straining, lifting, or blunt abdominal trauma. Additionally,
Mallory–Weiss tears can be iatrogenic, due to esophageal instrumentation, such
as nasogastric tube placement or upper endoscopy, or polyethylene glycol
administration. Despite frequent interventions, iatrogenic causes of
Mallory–Weiss tears are infrequent. Bleeding from Mallory–Weiss tears occurs
when the laceration involves either the esophageal arterial or the venous
plexus. Most frequently, the tears are single, but may be multiple in up to
one-quarter of patients.
Alcoholism
and hiatal hernias are the two main risk factors identified for the development
of Mallory–Weiss tears. Heavy alcohol use associated with emesis has been noted
in up to 80% of Mallory–Weiss syndrome. Similarly, hiatal hernia is found in
almost all patients with bleeding. It has been proposed that a higher pressure
gradient develops in the intra-thoracic portion of the stomach and G–E
junction, thus increasing acute distension and mucosal tears. Although age has
been postulated as a risk factor for development of Mallory–Weiss tears, the
majority occur in patients in their forties and fifties. It does appear that
age may be a predisposing factor for iatrogenic tears after endoscopy, likely
due to atrophic mucosa.
Presentation
The majority of patients present with hematemesis
often associated with epigastric, chest, or back pain. Classically, patients
will give a history of antecedent non-bloody emesis or retching but a
significant minority will give a history of bleeding with the initial emesis.
In the majority of cases, bleeding is self-limited, but lifethreatening
hemorrhage requiring blood transfusion, hemodynamic support, and endoscopic or
operative intervention may be required. A 1997 study identified active bleeding
at the time of endoscopy as a risk factor for higher transfusion rate and
portal hypertension or coagulopathy as a risk for re-bleeding.
Diagnosis
Early endoscopy is the diagnostic modality of choice
with Mallory–Weiss tears. Endoscopy is diagnostic and can rule out other causes
of upper gastrointestinal bleeding, such as varices, esophageal lesions,
esophagitis, or ulcers. Additionally, endoscopy can be therapeutic. Most
lesions will heal within 48 h, so delayed esophagoscopy may not be diagnostic.
Endoscopically, Mallory–Weiss tears appear as longitudinal lacerations through
the mucosa, occasionally exposing the muscular layer of the esophagus (Fig. 1).
These tears can be non-bleeding, actively bleeding, or covered in clotted
blood.
Fig. 1 Endoscopic image of Mallory–Weiss tear
Treatment
Although up to 70% of patients with Mallory–Weiss
syndrome ultimately require blood transfusion, the majority of lacerations heal
spontaneously. As with any GIB patient, large-bore intervenous access should be
obtained and adequate intervenous fluid resuscitation should be instituted.
Coagulopathy should be reversed, with vitamin K or fresh frozen plasma as
indicated. Patients should be closely monitored for hemodynamic changes. Most
patients are started on proton pump inhibitors, although their effectiveness
for Mallory–Weiss tears is doubtful. Additionally, patients should be put on
bowel rest during their initial observation.
Early endoscopy is critical in the diagnosis and
treatment of patients with Mallory–Weiss tears. If, on endoscopy, active
bleeding is not observed, no endoscopic therapy is indicated and the patient
should be observed for re-bleeding for 48 h. If bleeding is observed,
endoscopic therapy (such as injections, electrocautery, or clipping) is the
first-line treatment of patients with on-going bleeding from Mallory–Weiss
tears. Injection of epinephrine, ethanol, or other sclerosing agents is the
most commonly used treatment (Fig. 2). Epinephrine (1:10,000) with or without
an additional sclerosing agent (such as polidocanol) appears to be very
effective with an approximately 5% re-bleeding rate. Thermal coagulation with
either bipolar or multipolar electrocautery (Fig. 3) has also been described.
Fig. 2 Injection of epinephrine via needle catheter in
esophagus
Fig. 3 Multipolar electrocautery catheter (Bicap)
Although
this treatment modality may be used, caution must be exhibited. The technique
of electrocoagulation is similar to that used for bleeding ulcers but usually
less tamponade force and lower total energy because of the smaller size area
and to avoid perforation (e.g., bipolar probe at 15–18W, short pulse such as
one second and moderate tamponade force often laterally with a stiff probe).
Electrocautery should be avoided in patients with portal hypertension and
esophageal varices, as this may worsen bleeding and may be life threatening.
Additionally, because the esophagus lacks a serosal layer, coagulation may
cause full thickness injury and perforation and should be used judiciously.
Electrocautery is best indicated in small, limited lesions, where minimal
electrocautery can be used.
Multiple small trials have reported excellent results
with the application of hemoclips (Figs. 4a, 4b) to Mallory–Weiss tears. These
studies reported excellent hemostasis and minimal to no re-bleeding. Despite
this, a recent meta-analysis of endoscopic clipping for acute non-variceal
upper gastrointestinal bleeding reported that clipping alone was not superior
to other endoscopic modalities. These results may be slightly skewed due to the
fact this analysis contained a majority of patients with lesions other than
Mallory–Weiss tears. Variceal banding has been reported for treatment of
Mallory–Weiss tears with good results for these patients. Just as with
treatment of bleeding ulcers, multiple endoscopic therapeutic techniques have
been shown to be effective and the technique used should probably be dependent
upon the experience and comfort level of the endoscopist.
Re-bleeding is treated with repeat endoscopic
treatment. Patients with refractory bleeding can be treated with angiographic
embolization, balloon tamponade, or intervenous infusion of vasopressin. Very
rarely, patients with refractory bleeding will require surgical intervention.
This usually consists of creating a longitudinal esophagotomy and over-sewing
the bleeding vessels. With the improvement of endoscopic therapies, surgery is
the last line therapy and is required in a very small percentage of patients.
After successful intervention, the patient should be observed for bleeding for
at least 48 h.
Fig. 4a Mallory–Weiss tear in patient with acute
bleeding
Fig. 4b Multiple endoclips applied to Mallory–Weiss tear
Conclusion
Mallory–Weiss syndrome is characterized by bleeding
esophageal lacerations most commonly caused by forceful retching. Although up
to 70% of patients received blood transfusions, the majority of bleeding is
self-limited and requires no intervention. Early endoscopy is the diagnostic and
therapeutic modality of choice. If no bleeding is visualized, the patient can
be observed for 48 h. If the laceration is actively bleeding, endoscopic
therapies, such as sclerotherapy, electrocautery, or clipping, are highly
effective with a re-bleeding rate of approximately 5%.
Methods to control bleeding
(hemostasis)
There are two basic methods to control of bleeding: operative and conservative. They all also divided on temporary and final methods of hemostasis.
Temporary methods to control of
bleeding of one’s nature are mechanical.
There
are applying:
-
An applying a arresting bleeding tourniquet (fig. 2);
-
Digital compression of artery;
-
The maximal flexion or a raised position of an extremity;
-
A pressure bandage;
-
A tamponade of a wound;
- Applying
clamp on bleeding vessel;
- A temporarily shunting.
Rules
of tourniquet application:
1.
Before applying a tourniquet elevate an extremity;
2.
Arresting bleedind toutniquet is applied proximally of wounds (during an
arterial bleeding), as closer as possible to it;
3.
Under arresting bleeding toutniquet it is necessary to line a material
(clothes);
4.
In the time of applying of arresting bleedind toutniquet make two - three
rounds, uniformly stretching it. Thus rounds of arresting bleedind toutniquet
should not lie down one on another.
5.
After end of procedure it is necessary to indicate an exact times of an
applying a tourniquet;
6.
The part of a body where tourniquet is applied should be accessible to
examination;
7.
The tourniquet has to be on that area of an extremity where there is one bone.
Criterias
of a correct applying a tourniquet are:
-
Control of haemorrhage;
-
Absence of a peripheric pulsation;
- Colourless (pale) and cold an extremity.
Very important that the tourniquet cannot stay more than two hours on the low extremities and 1,5 hours on upper. In the other case the development of necrosis of an extremity is probably. As a result of a long ischemia of an extremity the necrosis is arised. If necessary long transportation of the victim, doctor must to loosen the tourniquet each hour approximately on 10 - 15 minutes. At this time replace this method with other temporary method control to bleeding (for example - digital compression of artery).
Final methods to control bleeding
(final hemostasis)
Depending
on the nature of methods which are applied, the last are divided on mechanical,
physical (thermal), chemical and biological.
Mechanical:
·
Ligating a vessel in a wound;
·
Ligating a vessel at a distance (fig. 3);
·
Under-runing a bleeding vessel;
·
Vasoversion, a crush of a vessel;
·
Tamponade of a wound (cavity), a pressure bandage (serves
as a temporary method, but sometimes - as a final method to control bleeding);
·
Embolization of vessel;
·
Special methods (splenectomy at a parenchymatous bleeding
from a lien, a resection of a stomach at a bleeding from a ulcer or a tumour, a
lobectomy at a pulmonary bleeding, Blaekmor’ probe, etc.);
·
A vascular
seam, reconstruction of vessels.
Physical:
·
Action of low temperature (a local hypothermia, a
cryosurgery);
·
Action of high temperature (action of hot solutions, a
electrocoagulation, a laser photocoagulation, a plasma scalpel).
Chemical:
-
Local hemostatics (hydrogen peroxide, vasoconstrictive
agents, inhibitors of a fibrinolysis, preparations of gelatin, wax);
-
Hemostatics of absorbtion action (inhibitors of a
fibrinolysis, calcium chloride, an agent which accelerate formation of a
thromboplastin, substances of specific action - Pituitrinum, synthetic
analogues of vitamin K, substances which normalize a vessel wall permeability).
Biological:
-
Packing the bleeding wound with the patient’s own tissues
(omentum, muscular tissue, subcutaneous fat, fascia);
-
Transfusion of small quantities of blood, fresh plasma,
serum, thrombocytes, fibrinogen, etc., injection of protrombin complex –
concentrated coagulation factors II – VII – IX – X, antihemophilic globulin A;
-
Injection of vitamins;
-
Intramuscular injection of human or animal serum;
-
Local application of blood derivates (trombin,
haemostatic sponge, isogenic fibrinous film, biological antiseptic pack, etc.).