4.2 Bacteraemia (septic shock)
Also named, Toxic shock, and Distributive shock.
It is diagnosed more often in surgical practice today.
There are more aged, immune-compromised patients in hospital.
There are more implants and interventions.
There are more post trauma admissions.
*Septic Shock
Septic shock is the second most frequent cause of shock in the surgical patients.
Invasive bacterial infection represents the most common cause of septic shock, with the most likely sites of infection being the lungs, abdomen, and urinary tract.
Bacterial products cause release of cytokines, tumor necrosis factor-alpha (TNF –alpha) and thromboxanes platelet activating factor, prostaglandin’s etc.
The inflammatory milieu induces several circulatory changes
First, myocardial depression is often evident despite an increase in cardiac index. Several factors contribute to cardiac dysfunction, including biventricular dilatation, myocardial hypo-responsiveness to catecholamine, and diastolic dysfunction.
-Together these phenomena result in a significant reduction in ejection fraction and a sub-optimal response to volume infusion that persists for as long as 10 days.
-The increase in cardiac index despite a reduction in myocardial contractility occurs as a result of a profound reduction in vasomotor tone, the principal cause of hypotension in septic shock.
-The reduction in venous tone leads to pooling of blood in large capacitance vessels, effectively reducing circulating blood volume.
-Several microcirculatory changes also occur distinct from change in vasomotor tone.
These also play a role in the manifestations of septic shock.
The mediator environment of sepsis,
-results in activation of the coagulation cascade,
-leading to micro-thrombus formation, leading to capillary plugging.
This micro-vascular occlusive phenomenon induces the opening of arteriovenous shunts, effectively depriving tissues of adequate perfusion.
Several pro-inflammatory mediators also increase neutrophil endothelial adherence and subsequent exit of activated inflammatory cells into the interstitium where they induce tissue injury.
Increased vascular permeability results in edema which effectively increase the distance required to be covered for cellular oxygen delivery and the opening of arterio-venous shunts, induces cellular hypoxia.
Clinical
Early manifestations of severe sepsis, include, tachypnea, tachycardia, oliguria, and changes in mental status.
-Thus, these simple clinical features should be considered evidence of impending shock in those at risk.
-These clinical features may be followed by the onset of fever and leukocytosis.
Early aggressive management is required to minimizing the morbidity and mortality of septic shock.
- The systemic vaso-dilation and increase in micro-vascular permeability result in patients to require large amount of intravenous fluid to restore a normal blood pressure.
- Vasopressors used are dopamine, epinephrine, or nor-epinephrine if there is an inadequate blood pressure response to fluid resuscitation.
- In-patients not responding to fluid infusion or those with underlying cardiac of renal disease, the use of pulmonary artery catheter is indicated.
- The resuscitation process is incomplete without all measures to reverse the infections process as early as possible.
- The correct choice of antibiotic or antibiotic combination is required.
- If the infection source is an abscess or there is a prior soiling of the pleural or peritoneal cavities, then either drainage or control of contamination is mandatory.
- Similarly, necrotic, infected tissue requires aggressive debridement.*
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
Wednesday, July 14, 2010
Wednesday, July 7, 2010
SHADES OF SHOCK
4. Shock Syndromes
The events of shock may result from:
4.1 Oligemic (Hypo-volemic) shock due to decrease in circulating
blood volume resulting from :
i) Hemorrhage (internal or external)
ii) Loss of fluid as in burns,trauma(Third space) or
dehydration
iii) Decreased extra-cellular fluid because of hypo-natreamia
as in Addison's disease
Hypovolemic shock occurs most often following trauma resulting
in blood loss.
It also occurs following GI bleeds, or a leak from an aneurysm.
Plasma volume losses can occur in trauma, burns, intestinal obstruction, diarrhea and heat stoke.
*Hypovolemic shock
Hypovolemic shock is the most common cause of shock. It may occur as a result of one of two events:
1. hemorrhage, representing intravascular volume decrease through the loss of whole blood or
2. loss of plasma volume through extra-vascular fluid loss or fluid loss from gastrointestinal, urinary tracts, and insensible loss.
-Hemorrhage is the form of volume loss that is common in practice can be measured and studied and thus is the better understood form of shock.
-Extra-vascular internal fluid leak, also referred to as “third space” fluid losses, is frequently unnoticed as a cause of shock.
-Third space fluid losses are the principal cause of volume loss in the early postoperative period and in local inflammatory processes, such as pancreatitis, in which local changes in capillary permeability result in fluid extravasations from the intravascular space into the interstitial space.
-Fluid leak is the principal cause of shock in patients with small bowel obstruction.
In this case, volume loss results from fluid loss into the interstitial space, bowel lumen, and exudation of fluid into the peritoneal cavity.
-The clinical manifestations of nonhemorrhagic forms of hypovolemic shock are the same as with hemorrhage, although they can be more slow in onset.
-The physiological responses of the body to hypovolemic shock are aimed at maintenance of cerebral and coronary perfusion and improving the circulating blood volume. The major compenstory mechanisms include
- An increase in sympathetic activity
- Release of stress hormones and
- Volume improvement through restoration of interstitial fluid, mobilization of intracellular fluid, saving of fluids and electrolytes by the kidney.
The clinical picture reflects this intense adreno-sympathetic response and renal conservation of fluid.
-Micro-vascular low perfusion of some vascular beds of organs results from a combination of low intravascular blood volume, diminished cardiac output resulting from a reduction in venous return and preload, and compensatory vaso-constriction.*
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review.
The events of shock may result from:
4.1 Oligemic (Hypo-volemic) shock due to decrease in circulating
blood volume resulting from :
i) Hemorrhage (internal or external)
ii) Loss of fluid as in burns,trauma(Third space) or
dehydration
iii) Decreased extra-cellular fluid because of hypo-natreamia
as in Addison's disease
Hypovolemic shock occurs most often following trauma resulting
in blood loss.
It also occurs following GI bleeds, or a leak from an aneurysm.
Plasma volume losses can occur in trauma, burns, intestinal obstruction, diarrhea and heat stoke.
*Hypovolemic shock
Hypovolemic shock is the most common cause of shock. It may occur as a result of one of two events:
1. hemorrhage, representing intravascular volume decrease through the loss of whole blood or
2. loss of plasma volume through extra-vascular fluid loss or fluid loss from gastrointestinal, urinary tracts, and insensible loss.
-Hemorrhage is the form of volume loss that is common in practice can be measured and studied and thus is the better understood form of shock.
-Extra-vascular internal fluid leak, also referred to as “third space” fluid losses, is frequently unnoticed as a cause of shock.
-Third space fluid losses are the principal cause of volume loss in the early postoperative period and in local inflammatory processes, such as pancreatitis, in which local changes in capillary permeability result in fluid extravasations from the intravascular space into the interstitial space.
-Fluid leak is the principal cause of shock in patients with small bowel obstruction.
In this case, volume loss results from fluid loss into the interstitial space, bowel lumen, and exudation of fluid into the peritoneal cavity.
-The clinical manifestations of nonhemorrhagic forms of hypovolemic shock are the same as with hemorrhage, although they can be more slow in onset.
-The physiological responses of the body to hypovolemic shock are aimed at maintenance of cerebral and coronary perfusion and improving the circulating blood volume. The major compenstory mechanisms include
- An increase in sympathetic activity
- Release of stress hormones and
- Volume improvement through restoration of interstitial fluid, mobilization of intracellular fluid, saving of fluids and electrolytes by the kidney.
The clinical picture reflects this intense adreno-sympathetic response and renal conservation of fluid.
-Micro-vascular low perfusion of some vascular beds of organs results from a combination of low intravascular blood volume, diminished cardiac output resulting from a reduction in venous return and preload, and compensatory vaso-constriction.*
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review.
Wednesday, June 30, 2010
SHOCKING EFFECTS
2. LOCAL INJURY EFFECTS
2.1. The most significant effect of injury, to any part of the
body, is a decrease of circulating body fluid volume due to
-Blood loss,
-Edema fluid loss.
2.2. The tissues in the part that receives the physical injury
will initiate an inflammatory response.
2.3 Inflammation starts with an increased capillary permeability
in the injured area, resulting in exudation of the edema fluid in
the interstitial space.
2.4. If the injured part is considerable in size, there will be a
considerable retention of the fluid in this injured area creating
a third space, besides the intracellular and extra cellular spaces.
3. THE PERFUSION PUMP FACTORS
The principal central physiological factors that affect our
circulation is the following:-
3.1 Pre-load or the initial cardiac muscle fiber stretch, just
before contraction is an important determinant of cardiac muscle
functions (Starlings Law).
This is the end diastolic volume (filling) of the ventricle.
3.2 After-load. Cardiac function is affected by the
resistance, against which the heart muscle has to work in both
the pulmonary and systemic circuits.
This is the arterial resistance (pressure)
3.3 Contractility of cardiac muscle.
This is the reserve ability of the heart muscle to work efficiently
under conditions of pre-load and after-load.
3.4 Lastly it is the Heart rate.
The rate increases the cardiac output without increase in the
stroke volume.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
2.1. The most significant effect of injury, to any part of the
body, is a decrease of circulating body fluid volume due to
-Blood loss,
-Edema fluid loss.
2.2. The tissues in the part that receives the physical injury
will initiate an inflammatory response.
2.3 Inflammation starts with an increased capillary permeability
in the injured area, resulting in exudation of the edema fluid in
the interstitial space.
2.4. If the injured part is considerable in size, there will be a
considerable retention of the fluid in this injured area creating
a third space, besides the intracellular and extra cellular spaces.
3. THE PERFUSION PUMP FACTORS
The principal central physiological factors that affect our
circulation is the following:-
3.1 Pre-load or the initial cardiac muscle fiber stretch, just
before contraction is an important determinant of cardiac muscle
functions (Starlings Law).
This is the end diastolic volume (filling) of the ventricle.
3.2 After-load. Cardiac function is affected by the
resistance, against which the heart muscle has to work in both
the pulmonary and systemic circuits.
This is the arterial resistance (pressure)
3.3 Contractility of cardiac muscle.
This is the reserve ability of the heart muscle to work efficiently
under conditions of pre-load and after-load.
3.4 Lastly it is the Heart rate.
The rate increases the cardiac output without increase in the
stroke volume.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
Wednesday, June 23, 2010
SHOCK- DEFINING MOMENTS
SHOCK
1. DEFINITION
The chief cause leading to shock is a lack of tissue
perfusion with oxygenated blood.
-Shock is low blood pressure, which is referred to as hypotension, but it also shows a continued inadequate tissue perfusion with O2.
-Thus the metabolic requirements of the tissues are not met.
-These requirements include supply of nutrients including O2, and removal of waste products.
1.1 If shock is treated in time cellular injury is limited.
1.2 If not treated irreversible widespread cell injury occurs
leading to multiple organ dysfunction and failure.
*Overview
-Shock is a clinical syndrome resulting from inadequate tissue perfusion.
-The decrease of delivery of requirement and the cellular unmet demand lead to cellular injury.
-Inadequate oxygen delivery is the main cause of shock states, the clinical manifestations of shock are caused by end organ dysfunction because of lower perfusion in spite of the body’s compensatory response.
-The continuing insufficient supply of oxygen to cells following sympathetic and neuron-endocrine interventions is cause of the symptoms and signs of shock.
-Timely restoration of perfusion and oxygen delivery usually reverse the shock state.
However the persistence or progression of shock may occur as a result of an ongoing undiagnosed perfusion defect or irreversible cellular injury, or a combination of the two phenomena.
-In addition, there is substantial clinical and laboratory evidence suggesting that cellular injury leads to production of pro-inflammatory chemical mediators that may further compromise perfusion through functional and structural changes in the microvasculature.
-This form of secondary injury further reduces perfusion, creating a vicious cycle of cellular injury leads to impaired perfusion that further increases cellular injury.
-Last in total body hypo-perfusion there is activation of potent inflammatory cells that may lead to the systemic inflammatory response syndrome (SIRS).
-It is suggested that persistence of SIRS, through the total body cellular dysfunction, may be the cause for the development of the multiple organ dysfunction syndrome (MODS).*
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
1. DEFINITION
The chief cause leading to shock is a lack of tissue
perfusion with oxygenated blood.
-Shock is low blood pressure, which is referred to as hypotension, but it also shows a continued inadequate tissue perfusion with O2.
-Thus the metabolic requirements of the tissues are not met.
-These requirements include supply of nutrients including O2, and removal of waste products.
1.1 If shock is treated in time cellular injury is limited.
1.2 If not treated irreversible widespread cell injury occurs
leading to multiple organ dysfunction and failure.
*Overview
-Shock is a clinical syndrome resulting from inadequate tissue perfusion.
-The decrease of delivery of requirement and the cellular unmet demand lead to cellular injury.
-Inadequate oxygen delivery is the main cause of shock states, the clinical manifestations of shock are caused by end organ dysfunction because of lower perfusion in spite of the body’s compensatory response.
-The continuing insufficient supply of oxygen to cells following sympathetic and neuron-endocrine interventions is cause of the symptoms and signs of shock.
-Timely restoration of perfusion and oxygen delivery usually reverse the shock state.
However the persistence or progression of shock may occur as a result of an ongoing undiagnosed perfusion defect or irreversible cellular injury, or a combination of the two phenomena.
-In addition, there is substantial clinical and laboratory evidence suggesting that cellular injury leads to production of pro-inflammatory chemical mediators that may further compromise perfusion through functional and structural changes in the microvasculature.
-This form of secondary injury further reduces perfusion, creating a vicious cycle of cellular injury leads to impaired perfusion that further increases cellular injury.
-Last in total body hypo-perfusion there is activation of potent inflammatory cells that may lead to the systemic inflammatory response syndrome (SIRS).
-It is suggested that persistence of SIRS, through the total body cellular dysfunction, may be the cause for the development of the multiple organ dysfunction syndrome (MODS).*
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
Wednesday, June 16, 2010
BLOOD DOWNSIDE 2
7.3.2 HEPATITIS
Hepatitis B and C can be transmitted through blood transfusion.
Screening technique once again can increase the rate of detection
and cut the risk of transmission of the virus.
7.3.3 TRANSMISSION OF TROPICAL DISEASES
Malaria can also occur as a result of transfusion in our country. Donor screening procedures and history taking can limit this mode of transmission
7.4 MASSIVE TRANSFUSION
Changes are expected if more than 10 unit of blood are
transfused in 24 hours.
These effects are because of changes that occur in the blood
stored at 1 to 6oC in the blood bank.
-Leakage of intracellular Potassium from the RBC results in high
potassium in the plasma of stored blood.
-Decrease in pH and decrease in intracellular ATP also occur in stored blood.
-Affinity of RBC for oxygen (slow release of O2) and degeneration of white cells and platelets is observed in stored blood.
-There are also changes in clotting factor V and VIII leading to bleeding disorders.
-Blood stored for several days is devoid of functioning platelets. Therefore, there is dilutional thrombocytopenia
7.4.1 THERMAL LOAD
When large quantity of blood is transfused and blood is not
warmed there is excessive heat loss resulting in hypothermia.
Patient’s core temperature may fall below 34oc and the blood does
not clot normal.
Hypothermia slows citrate metabolism and reduces oxygen release by the hemoglobin
This effect can be counteracted if blood is warmed before
Transfusion.
7.4.2 ACID BASE CHANGES
There is usually alkalosis after massive transfusion.
Sodium citrate, (the anti-coagulant in the stored blood) is converted
into Sodium Bicarbonate in the liver.
The post transfusion pH may range from 7.48 to 7.50 and there is increased excretion of Potassium.
7.4.3 OTHER CHANGES DUE TO CITRATE
The citrate received with massive transfusion can also lead to
decreased level of calcium because the citrate binds ionized
calcium lowering the plasma calcium levels, this effects the
blood pressure (hypotension), narrowing pulse pressure, increase
central venous pressure.
The EGG shows a prolonged QT interval.
7.4.4 CHANGES IN POTASSIUM
This occurs because of leakage of potassium from the RBC into the
plasma.
This high potassium may cause rise in T waves in ECG.
In *association with hypocalcaemia this may alter cardiac
function.
7.4.5 HOMEOSTASIS
Massive transfusion leads to a decrease in a number of viable
platelets, since the stored blood has a very few platelets.
The platelet count may fall in cases of massive transfusion.
The PT and aPTT provides a reliable indicator for deciding whether FFP
is needed for the treatment of this effect.
Any questions be sent to drmmkapur@gmail.com you will receive a response
All earlier posts are stored in archives for you’re access and review
Hepatitis B and C can be transmitted through blood transfusion.
Screening technique once again can increase the rate of detection
and cut the risk of transmission of the virus.
7.3.3 TRANSMISSION OF TROPICAL DISEASES
Malaria can also occur as a result of transfusion in our country. Donor screening procedures and history taking can limit this mode of transmission
7.4 MASSIVE TRANSFUSION
Changes are expected if more than 10 unit of blood are
transfused in 24 hours.
These effects are because of changes that occur in the blood
stored at 1 to 6oC in the blood bank.
-Leakage of intracellular Potassium from the RBC results in high
potassium in the plasma of stored blood.
-Decrease in pH and decrease in intracellular ATP also occur in stored blood.
-Affinity of RBC for oxygen (slow release of O2) and degeneration of white cells and platelets is observed in stored blood.
-There are also changes in clotting factor V and VIII leading to bleeding disorders.
-Blood stored for several days is devoid of functioning platelets. Therefore, there is dilutional thrombocytopenia
7.4.1 THERMAL LOAD
When large quantity of blood is transfused and blood is not
warmed there is excessive heat loss resulting in hypothermia.
Patient’s core temperature may fall below 34oc and the blood does
not clot normal.
Hypothermia slows citrate metabolism and reduces oxygen release by the hemoglobin
This effect can be counteracted if blood is warmed before
Transfusion.
7.4.2 ACID BASE CHANGES
There is usually alkalosis after massive transfusion.
Sodium citrate, (the anti-coagulant in the stored blood) is converted
into Sodium Bicarbonate in the liver.
The post transfusion pH may range from 7.48 to 7.50 and there is increased excretion of Potassium.
7.4.3 OTHER CHANGES DUE TO CITRATE
The citrate received with massive transfusion can also lead to
decreased level of calcium because the citrate binds ionized
calcium lowering the plasma calcium levels, this effects the
blood pressure (hypotension), narrowing pulse pressure, increase
central venous pressure.
The EGG shows a prolonged QT interval.
7.4.4 CHANGES IN POTASSIUM
This occurs because of leakage of potassium from the RBC into the
plasma.
This high potassium may cause rise in T waves in ECG.
In *association with hypocalcaemia this may alter cardiac
function.
7.4.5 HOMEOSTASIS
Massive transfusion leads to a decrease in a number of viable
platelets, since the stored blood has a very few platelets.
The platelet count may fall in cases of massive transfusion.
The PT and aPTT provides a reliable indicator for deciding whether FFP
is needed for the treatment of this effect.
Any questions be sent to drmmkapur@gmail.com you will receive a response
All earlier posts are stored in archives for you’re access and review
Thursday, June 10, 2010
DOWNSIDE OF BLOOD FOR BLOOD
6. The Blood GROUPS
There are four types of groups:
1. Group A (red cells contain A agglutinogens, serum contain
Anti B agglutinins)
2. Group B (red cells contain B agglutinogens, serum contain
Anti A agglutinins)
3. Group AB (red cells contain both A and B agglutinogens,
serum contains no agglutinins)
4. Group O (red cells have no A or B agglutinogens, serum
contains both Anti A and Anti B agglutinins)
7. COMPLICATIONS OF TRANSFUSION
7.1 ABO Incompatibility
The most important complication resulting in loss of life is the
transfusion reaction, because of A, B, O incompatibility.
Most of these are events that result from clerical errors
-when the correct cross match has not been made or
-correct group had not been indicated on supplied blood.
In many cases the correct patient has not been
Identified in the ward.
These errors are preventable by installing ward and laboratory
procedures wherein no errors can occur.
When such transfusion reaction is suspected the transfusion should
be stopped and the urine be tested for Hemoglobin.
The blood bank should recheck the samples and record the event to identify the cause of the mismatch.
The patient should receive fluids to correct hypotension and
maintain renal blood flow.
Mannitol may be useful for diuresis.
7.2 IMMUNE REACTIONS
7.2.1 HEMOLYTIC
These reactions occur as a delayed reaction after the
transfusion has been completed.
-There is fall in hematocrit and it is accompanied by fever and
Jaundice.
-This jaundice may be caused by the antibodies to earlier
transfusions.
It may also be because of mishandled blood packs or infected blood packs.
7.2.2 NON-HEMOLYTIC REACTIONS
Erythma,
Urticaria,
Pruritus, occur within a few minutes of start
of transfusion.
-These are allergic reactions and the symptoms are due to release of Histamine and Serotonin as result of antigen-antibody reaction.
Transfusion is slowed down, and anti-histamine is given.
If no progress of symptoms occurs the transfusion can be continued.
7.2.3 ANAPHYLACTIC REACTION
The symptoms include
* Respiratory distress Bronchospasm
* Hypertension later Hypotension
* Subcutaneous edema
These are caused by antigen-antibody reaction and complement
activation and treated by:
1. Stop transfusion
2. Start isotonic saline
3. Anti-Histamine intravenously
4. Cortico-steroid 100 mg. hydrocortisone IV
5. Oxygen
6. Give diuretics eg. Furosemide. IV
7.3 TRANSMISSION OF DISEASE
Viral and bacterial infection can be transmitted by blood
transfusion.
This is possible if proper screening procedures for
donors are not conducted.
7.3.1 HUMAN IMMUNODEFICIENCY VIRUS
If screening of donar for HIV is not conducted this virus can be
transmitted through blood transfusion.
Awareness of prevalence of HIV in the population and screening
Procedure will bring down this mode of transmission.
Any questions be sent to drmmkapur@gmail.com
There are four types of groups:
1. Group A (red cells contain A agglutinogens, serum contain
Anti B agglutinins)
2. Group B (red cells contain B agglutinogens, serum contain
Anti A agglutinins)
3. Group AB (red cells contain both A and B agglutinogens,
serum contains no agglutinins)
4. Group O (red cells have no A or B agglutinogens, serum
contains both Anti A and Anti B agglutinins)
7. COMPLICATIONS OF TRANSFUSION
7.1 ABO Incompatibility
The most important complication resulting in loss of life is the
transfusion reaction, because of A, B, O incompatibility.
Most of these are events that result from clerical errors
-when the correct cross match has not been made or
-correct group had not been indicated on supplied blood.
In many cases the correct patient has not been
Identified in the ward.
These errors are preventable by installing ward and laboratory
procedures wherein no errors can occur.
When such transfusion reaction is suspected the transfusion should
be stopped and the urine be tested for Hemoglobin.
The blood bank should recheck the samples and record the event to identify the cause of the mismatch.
The patient should receive fluids to correct hypotension and
maintain renal blood flow.
Mannitol may be useful for diuresis.
7.2 IMMUNE REACTIONS
7.2.1 HEMOLYTIC
These reactions occur as a delayed reaction after the
transfusion has been completed.
-There is fall in hematocrit and it is accompanied by fever and
Jaundice.
-This jaundice may be caused by the antibodies to earlier
transfusions.
It may also be because of mishandled blood packs or infected blood packs.
7.2.2 NON-HEMOLYTIC REACTIONS
Erythma,
Urticaria,
Pruritus, occur within a few minutes of start
of transfusion.
-These are allergic reactions and the symptoms are due to release of Histamine and Serotonin as result of antigen-antibody reaction.
Transfusion is slowed down, and anti-histamine is given.
If no progress of symptoms occurs the transfusion can be continued.
7.2.3 ANAPHYLACTIC REACTION
The symptoms include
* Respiratory distress Bronchospasm
* Hypertension later Hypotension
* Subcutaneous edema
These are caused by antigen-antibody reaction and complement
activation and treated by:
1. Stop transfusion
2. Start isotonic saline
3. Anti-Histamine intravenously
4. Cortico-steroid 100 mg. hydrocortisone IV
5. Oxygen
6. Give diuretics eg. Furosemide. IV
7.3 TRANSMISSION OF DISEASE
Viral and bacterial infection can be transmitted by blood
transfusion.
This is possible if proper screening procedures for
donors are not conducted.
7.3.1 HUMAN IMMUNODEFICIENCY VIRUS
If screening of donar for HIV is not conducted this virus can be
transmitted through blood transfusion.
Awareness of prevalence of HIV in the population and screening
Procedure will bring down this mode of transmission.
Any questions be sent to drmmkapur@gmail.com
Thursday, June 3, 2010
BLOOD FOR BLOOD
5. BLOOD TRANSFUSION
The varieties of hemorrhages have been dealt with in detail in chapter on Shock(Chap3).
We need to discuss here some clinical methods for assessing the
amount of blood loss so as to start treatment.
To estimate blood loss in the ward or emergency room:
* Swabs can be counted and weighed to estimate blood loss
* The clots can also be weighed to calculate blood lost
* In closed wounds, a moderate swelling in the leg may indicate
a loss of 1000-1500 cc of blood
* A similar swelling in the thigh (fracture femur) may
indicate a loss of 1000-2000cc
* Fracture pelvis may indicate a loss of >2000cc
Blood loss of <20% need not be replaced with whole blood.
-Immediate circulating fluid needs are provided by the transfer of fluid from the extra-vascular compartments.
-Protein lost in the blood is replaced by the body protiens in days
-RBC are replaced in weeks.
-Blood loss of 20-25% can be replaced by saline,
-loss of 30-35% may require replacement with plasma substitutes.
-When loss of 50% or more occurs replacement with whole stored blood is
required.
BLOOD is required in all cases of acute blood loss:
* Trauma + haemorrhage-(fracture)
* Intra-operative
* Post-operative
* In cases of deep burns
* In cases of bleeding disorders
5.1 HOMOLOGUS BLOOD
Stored blood is obtained from donors and kept in bags of 300cc.
Each donor needs to be carefully screened to limit the risk of
transmission of disease to the recipient.
5.2 AUTOLOGOUS BLOOD
Patient can donate his own blood within 5 weeks prior to the
surgery.
This blood can then be used at the time of surgery.
Blood lost during surgery can also be collected at that time
Washed, filtered and re-infused.
5.3 Blood Grouping and Cross Matching
Transfusion of blood require arrangements with the blood
bank
-to group patient's blood and
-cross match sample of blood
with sample of the same group in the blood bank.
-For this purpose a sample of blood has to be obtained from the
patient.
-All red cells contain agglutinogens (A and B).
-The serum contains Agglutinins (Anti A and Anti B).
5.4 Rh Factors
This is an antigen found in Red Cells and human red cells can be
either Rh+ or-.
Antibodies in the serum develop if Rh positive cells are
injected in Rh negative.
At the 1st repeat transfusion no problem may arise but subsequently
transfusion may produce Haemolysis.
Approximately 85% of the population is Rh positive.
Before transfusion the red cells of the donor (stored blood) are
matched against the serum of the recipient (the patient)
Any questions be sent to drmmkapur@gmail.com
The varieties of hemorrhages have been dealt with in detail in chapter on Shock(Chap3).
We need to discuss here some clinical methods for assessing the
amount of blood loss so as to start treatment.
To estimate blood loss in the ward or emergency room:
* Swabs can be counted and weighed to estimate blood loss
* The clots can also be weighed to calculate blood lost
* In closed wounds, a moderate swelling in the leg may indicate
a loss of 1000-1500 cc of blood
* A similar swelling in the thigh (fracture femur) may
indicate a loss of 1000-2000cc
* Fracture pelvis may indicate a loss of >2000cc
Blood loss of <20% need not be replaced with whole blood.
-Immediate circulating fluid needs are provided by the transfer of fluid from the extra-vascular compartments.
-Protein lost in the blood is replaced by the body protiens in days
-RBC are replaced in weeks.
-Blood loss of 20-25% can be replaced by saline,
-loss of 30-35% may require replacement with plasma substitutes.
-When loss of 50% or more occurs replacement with whole stored blood is
required.
BLOOD is required in all cases of acute blood loss:
* Trauma + haemorrhage-(fracture)
* Intra-operative
* Post-operative
* In cases of deep burns
* In cases of bleeding disorders
5.1 HOMOLOGUS BLOOD
Stored blood is obtained from donors and kept in bags of 300cc.
Each donor needs to be carefully screened to limit the risk of
transmission of disease to the recipient.
5.2 AUTOLOGOUS BLOOD
Patient can donate his own blood within 5 weeks prior to the
surgery.
This blood can then be used at the time of surgery.
Blood lost during surgery can also be collected at that time
Washed, filtered and re-infused.
5.3 Blood Grouping and Cross Matching
Transfusion of blood require arrangements with the blood
bank
-to group patient's blood and
-cross match sample of blood
with sample of the same group in the blood bank.
-For this purpose a sample of blood has to be obtained from the
patient.
-All red cells contain agglutinogens (A and B).
-The serum contains Agglutinins (Anti A and Anti B).
5.4 Rh Factors
This is an antigen found in Red Cells and human red cells can be
either Rh+ or-.
Antibodies in the serum develop if Rh positive cells are
injected in Rh negative.
At the 1st repeat transfusion no problem may arise but subsequently
transfusion may produce Haemolysis.
Approximately 85% of the population is Rh positive.
Before transfusion the red cells of the donor (stored blood) are
matched against the serum of the recipient (the patient)
Any questions be sent to drmmkapur@gmail.com
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