A very narrative discussion over Shock & Haemorrhage, Blood Transfusion, Blood Products which is presented in seminers. A concise guideline of a vast chapter.
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
Surgical hemostasis is one of the pillars of modern surgery. Adequate hemostasis in a surgical patient involves a detailed perioperative clinical evaluation and investigation, and various intra operative techniques and options. Ensuring adequate surgical hemostasis reduces morbidity and mortality by modulating the metabolic response to trauma, decreasing the incidence of post operative anemia, reduces rates of surgical site infection and ultimately improving wound healing
Suture Materials and Suturing Techniques - Presented by Dr. Prasanjit Das and group as a part of Dhaka Dental College, OMS Department weekly presentation program.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
Surgical hemostasis is one of the pillars of modern surgery. Adequate hemostasis in a surgical patient involves a detailed perioperative clinical evaluation and investigation, and various intra operative techniques and options. Ensuring adequate surgical hemostasis reduces morbidity and mortality by modulating the metabolic response to trauma, decreasing the incidence of post operative anemia, reduces rates of surgical site infection and ultimately improving wound healing
Suture Materials and Suturing Techniques - Presented by Dr. Prasanjit Das and group as a part of Dhaka Dental College, OMS Department weekly presentation program.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
shock is the state of insufficient blood flow to the tissues of the body .it contains introduction, definition, stages of shock, types of shock, diagnostic evaluation, prognosis ,prevention, care for each stage.
This topic is under the General Principles of Surgery. It is very important for MBBS - Students. New method of resuscitation called the Damaged Control Resuscitation is carried out in controlling the hemorrhage.
a clinical syndrome that results from inadequate tissue perfusion.
Hypovolemic shock - Blood or fluid loss, both leading to a decreased circulating blood volume, diastolic filling pressure, and volume.
Cardiogenic shock - due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes
Extra-cardiac/obstructive shock - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in arteriolar/venular dilatation leading to a decrease in preload, with decreased, normal, or elevated cardiac output, depending on the presence of myocardial depression.
A lecture discussing the role of Echocardiography in the evaluation and management of patients with different types of shock. From cardiogenic to hypovolemic to obstructive and distributive shock. A very useful guide for intensivists, cardiologists and all acute care physicians.
A brief discussion over CA Cervix. All newest updates in management protocol and revised by reknowned gynecologistts. Very much helpful for both under and post graduate students/Doctors.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Shock:
Def: Shock is a systemic state of low tissue perfusion that is inadequate for
normal cellular respiration.
Shock is the most common and therefore the most important
cause of death of surgical patients. Death may occur rapidly
due to a profound state of shock, or be delayed due to the
consequences of organ ischaemia and reperfusion injury. It
is important therefore that every surgeon understands the
pathophysiology, diagnosis and priorities in management of
shock and haemorrhage.
3. Classification of Shock
Based on the Initiating Mechanism:
Type of Shock Cause
Hypovolemic Shock Hemorrhage, Vomiting, Diarrhoea, Third Spacing,
Burn, Crush injury, Diuretics
Cardiogenic Shock MI, Cardiac Dysrhythmias, Valvular HD, Blunt
Myocardial Injury, Cardiomyopathy
Obstructive Shock Cardiac Tamponade, Tension Pneumothorax,
Massive Pulmonary Embolism
Distributive Shock Septic Shock, Anaphylaxis, Spinal Cord Injury
Endocrine Shock Adrenal Insufficiency, Hypothyroidism,
Thyrotoxicosis
Based on the Severity:
Type of Shock Subtype
1. Compensated Shock -
2. Decompensated Shock Mild, Moderate, Severe
6. Pathophysiology of Shock
Cardiovascular
↓Preload & Afterload
▼
↑Sympathetic Activity
▼
Tachycardia with Systemic
Vasoconstriction
Renal
↓Perfusion in Kidney
▼
↓Urine Output
▼
Stimulates Renin Angiotensin axis
▼
Further Vasoconstriction with Sodium
& Water reabsorption
Endocrine
↑Vasopressin, Adrenalin, Cortisol
▼
Vasoconstriction with Sodium & Water
reabsorption
7. Hypovolemic Shock
Hypovolaemia is probably the most common form of
shock, and to some degree is a component of all other forms
of shock.
Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due
to haemorrhagic or nonhaemorrhagic causes. Nonhaemorrhagic causes include poor
fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhoea, urinary loss
(e.g. diabetes), evaporation, or ‘thirdspacing’
where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in
bowel obstruction or pancreatitis.
Classification:
Class Percentage of Blood loss
1 <15%
2 <15%-30%
3 <30%-40%
4 >40%
11. Investigation for Shock
Mostly Clinical by Assessment of Pt. condition:
1. Vitals: BP, HR, RR, Temp.
2. Sate of hydration
3. Urine Output
4. Rate & amount of bleeding if any
5. Proper History taking
Lab Investigations:
1. CBC
2. Coagulation profile
3. Blood sugar, S. Electrolyte, S. Urea, S. Creatinine
4. Blood Culture
5. Imaging: CXR, USG, CT, MRI
12. Shock - Mx
Management of shock at a glance:
Immediate Resuscitation:
1. Maintenance of airway – OP suction
2. Maintenance of breathing – O2 inhalation/Intubation
3. Maintenance of circulation – I/V Fluid (R/L or H/S)
4. Blood transfusion (PCV/WB) or Blood Vol. Expanders
(Hypovolemic Shock)
5. Catheterization
6. Broad Spectrum Antibiotics (Septic Shock)
7. H2 blocker/PPI
8. Tetanus Prophylaxis (TT/Tig) (RTA/Trauma)
Specific Measures:
1. Vasopressor/Ionotropic Support
2. Prevention of ARF (U/O kept 50ml/hour)
3. Excision of dead tissue or drainage of pus
Monitoring:
13. Dynamic Fluid Response
The shock status can be determined dynamically by the Cardiovascular response to
the rapid administration of a fluid bolus.
Amount of bolus: 250-500 ml over 5-10 mins.
Route: CV line.
Parameter Monitored: HR, BP, CVP.
Classification of Pt.:
a) Responders: Improved and sustained cardiovascular status, not actively loosing
fluid only require filling to normal volume status.
b) Transient Responders: Initially have improvement but gradually over 10-20mins
deteriorates with ongoing fluid loss.
c) Non Responders: No improvement with severe volume depletion and loss.
14. Consequences of Shock
(If unattended)
Unresuscitatable shock
Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’. Cell
death follows from cellular ischaemia and the ability of the body to compensate is lost. There is
myocardial depression and loss of responsiveness to fluid or inotropic therapy. The peripheries no
longer respond appropriately to vasopressor agents. Death is the inevitable result. Conversely, when
patients present in this late stage, and have minimal responses to maximal therapy.
Multiple organ failure
Multiple organ failure is defined as two or more failed organ systems. The result of prolonged
systemic ischaemia and reperfusion injury is endorgan damage and causes multiple organ failure. There is
no specific treatment for multiple organ failure. Management is supporting of organ systems, with
ventilation, cardiovascular support and haemofiltration/dialysis until there is recovery of organ function.
Multiple organ failure currently carries a mortality of 60% .
15. New Concept of End Point Resuscitation
Traditionally, patients have been resuscitated until they have a normal pulse, blood
pressure and urine output. However, these parameters are monitoring organ
systems whose blood flow is preserved until the late stages of shock .
According to new concept Resuscitation algorithm for end point are:
1. Base Deficit
2. Lactate
3. Mixed Venous O2 saturation
17. Haemorrhage
Def: Escape of blood from the vascular compartment to the exterior.
Classification:
a) According to source of Haemorrhage/Visibility:
- Arterial
- Venous
- Capillary
b) According to duration:
- Primary Haemorrhage
- Reactionary Haemorrhage
- Secondary Haemorrhage
c) According to site of bleeding:
- External/Revealed
- Internal/Concealed
d) According to mode of onset: e) According to nature of Attention:
- Acute - Surgical Haemorrhage
- Chronic - Non-Surgical Haemorrhage
18. Deference among various Haemorrhage
Traits Primary Hemorrhage Reactionery Hemorrhage Secondary Hemorrhage
Time of
Occurrence
Occurs at any time of
operation or trauma
Occurs within 24 hours of
primary haemorrhage (Usually
4-6 hours)
Occurs after 7-14 days of
primary haemorrhage
Cause Injury to blood vessel
during operation or
trauma
a) Slipping of ligature
b) Dislodgement of clot
c) Cessation of reflex
vasospasm
d) Normalization of BP
a) Infection
b) Sloughing of wall of
blood vessel
c) Pressure Necrosis
d) Maliganancy
Example During any operation Commonly occurs after:
a) Tonsillectomy
b) Thyroidectomy
c) Prostatectomy
d) Haemorrhoidectomy
In any type of surgery
where there is infection or
malignancy.
19. Pathophysiology
Haemorrhage got worsen by factors mentioned below:
1. Acute traumatic coagulopathy (ATC)
2. Acidosis due to hypoperfusion Called triad of death
3. Hypothermia
4. Dilution of coagulation factor by continuous bleeding
Incidence: Upto 25% of trauma Pt. develop ATC within minutes of injury. It is
associated with four fold increase in Mortality.
20. Diagnosis
Careful examination of the operation/trauma site Excessive swelling can be present
referring internal bleeding/Hematoma)
Carefully examination of the drain tube for excessive collection of blood.
Patient may be severely anemic.
Increased Pulse rate.
Decreased BP.
Temperature may be cold/normal.
Respiratory rate may be increased.
Reduced Urine output
Lab Investigation: HB%, HCT, ESR etc.
21. Management of Haemorrhage
Identify Haemorrhage:
a) External Haemorrhage: can be seen
b) Concealed Haemorrhage: Any shock should be assumed to be hypovolemic until
proven otherwise.
Immediate Resuscitative Maneuver:
a) Direct pressure over external haemorrhage site.
b) Airway and breathing should be assessed and controlled.
c) Large bore I/V access.
d) Blood drawn for cross matching.
Identify the site of Haemorrhage:
History:
a) Previous episodes
b) Known aneurysm
c) Non-Steroidal therapy/Drug history
22. Management of Haemorrhage
Examination:
a) Nature of blood (Fresh/Melaena)
b) Abdominal tenderness
c) External signs of injury
Investigation:
a) CXR, Pelvic x-ray, USG W/A
b) Diagnostic peritoneal aspiration
c) Computed Tomography (CT)
Haemorrhage Control:
a) Pt. moved rapidly to a place of Haemorrhage control.
b) Surgical intervention may need to be limited to the minimum necessary to stop
bleeding and control sepsis.
c) Definitive repairs can be delayed until Pt. is hemodynamically stable.
d) Once haemorrhage controlled, Pt. should be aggressively resuscitated, warmed and
coagulopathy corrected.
23. Management of Haemorrhage
Haemorrhage Control:
a) Anticipate & treat acute traumatic coagulopathy
b) Permissive hypotension until haemorrhage control
c) Limit crystalloid & colloid infusion to avoid dilutional coagulopathy
d) Damage control surgery to control haemorrhage and preserve physiology
24. Haemostasis during Surgery
Endoscopic:
a) Injection
b) Thermal & Photocoagulation
c) Banding
d) Balloon tamponed
Radiological: Embolization of bleeding vessel
Surgical:
• Position & rest: Elevation of the limb
• Pressure Packing:
a) Pressure dressing
b) Digital Pressure
c) Roller Bandage
d) Ribbon Bandage
e) Tourniquets (Pneumatic/Rubber)
f) Use of double balloon tamponade to control bleeding
from oesophageal varices
25. Haemostasis during Surgery
• Operative Technique:
a) Pressure by artery forceps/clips
b) Topical application of haemostatic agents (Gelatin sponge) or adrenalin
c) Coagulation with diathermy
d) Ligation with catgut/silk
e) Temporary occlusion of inflow vessels – Pringle maneuver
f) Grafting (Another vessel/Tephlon)
g) Whole or part of bleeding viscous may be excised, eg. Splenectomy
27. Blood Transfusion
Def: Introduction of blood or blood product in human body is called blood
transfusion.
The first successful transfusion in 1818. Although there was many incidence of
severe transfusion reactions but now infections or reaction is now very low.
28. Type of Blood Transfusion
Homologous Blood Transfusion: One person to another
Autologous: Derived from same individual
o Intra and Postoperative cell storage: Collection of blood shed from intraoperative wound & drain
then process the blood to remove plasma constituents.
Use: Major orthopedic surgery
Cardiovascular Surgery
Hepatic Surgery, e.g. Liver transplantation
Contraindication: Dirty wound, Active Infection, Malignancy
o Normal normovolaemic hemodilution: Anesthetist withdraws several packs of Pt. blood replacing
with Crystalloid or Colloid. Collected blood then reinfused during operation. This is useful when
anticipated blood loss is >1L and Pt’s HCT is relatively high.
o Preoperative autologous deposit (PAD): Predonate Pt’s own blood 3 weeks prior surgery, around
2-4 units are collected. HB% kept >10gm/dl with oral iron supplementation .
Use: Major orthopedic & gynecological surgery
Contraindication: Active infection, Unstable Angina, AS, Severe HTN
29. Blood Products
Whole Blood
Blood Components:
a) Packed Red Cell
b) White Cell (Buffy coat)
c) Platelet
Plasma Component:
a) Fresh Frozen Plasma (FFP)
b) Cryoprecipitate
c) Human Albumin Solution
d) Immunoglobulin
e) Coagulation Factor Concentrate:
Recombinant Factor VIII, Factor IX
Recombinant Factor VIIa
Fibrinogen Concentrate
32. Complication of Stored Blood
Hyperkalaemia
Reduced 2,3 DPG (Lt. shift of O2 dissociation curve)
Acidosis (pH 6.6-6.8)
Contain citric anticoagulant – Intoxication
Ammonia intoxication
Changes Occur in Stored Blood
Potassium lactate, Ammonia value rises
Labile clotting factor (V,VIII) diminished
2,3 DPG level remain adequate for 14 days but virtually absent @21 days
CPD Preservative gradually decrease the pH upto 6.5 at the end of 2nd week
Platelet becomes functionally inactivated when it is stored in 4˚C and after 3 days no
platelet remains viable
33. Criteria of Ideal Donor
Must have good health status
Unpaid volunteers
Age: Within18-65 years
Weight: >45 kg/ 100 lb.
Body Temperature: <99˚F
Pulse: 60-100 b/min
BP: Within normal range
Medical History:
• No H/O recent fever, tooth extraction within 3wks, Operation within 3months.
• Vaccination within 3 months
• At time of menstruation
• Any H/O heart disease or current pregnancy
Hematological History:
• Hb%: >12 gm/dl
• No H/O anemia, leukemia, coagulopathy
34. Screening before Transfusion
Compatibility Test:
a) Blood grouping
b) Cross matching
Screening Test:
a) Viral: HBsAg, Anti HCV strip test
b) Malaria Parasite
c) VDRL/Syphilis
d) HIV
35. Complication of Blood Transfusion
Complications from a Single Transfusion
Complications from a single transfusion
include:
● Incompatibility haemolytic transfusion
reaction
● Febrile transfusion reaction
● Allergic reaction
●Infection:
1. Bacterial infection (usually due to faulty
storage)
2. Hepatitis
3. HIV
4. Malaria
5. Air embolism
6. Thrombophlebitis
7. Transfusion related acute lung injury
(usually from FFP)
Complications from a Massive Transfusion
● Coagulopathy
● Hypocalcaemia
● Hyperkalaemia
● Hypokalaemia
● Hypothermia
● Iron overload (In repeated transfusion)
36. Management of Mismatched
Blood Transfusion
Symptoms
Feeling of something wrong
Restlessness
Anxiety
Headache
Pain & Heaviness in chest, lumber region,
Limbs
Pain venipuncture site
Fever
Rigors
Dyspnoea
Acute collapse
Rash, itch
Signs
Pallor
Raised Temperature
Rapid thread pulse
Low BP
Pulmonary Oedema (B/L Basal Creps)
Cervical vein engorgement
Cyanosis
Facial puffiness
Jaundice
Haemoglobunuria
Haemoglobinaemia
Oliguria F/B Uraemia
37. Management of Mismatched
Blood Transfusion
Immediate measures:
1. Stop blood transfusion immediately
2. Recheck Pt. identity against donor unit
3. Inj. Hydrocortisone Hemisuccinate (2vials I/V Stat)
4. Inj. Anti-Histamine
5. Maintain I/V access with 0.9% NaCl solution
6. Monitoring urine output by catheterization > if U/O is less than 1.5ml/kg/hour will insert
CVP line and give fluid > If CVP adequate and U/O still less than 1.5ml/kg/hour then,
frusemide (80-120mg)
7. If suspicion of bacterial contamination, broad spectrum antibiotic should started.
8. Contact senior Medical personnel for advice and inform transfusion department.
9. Contact blood transfusion laboratory before sending back blood pack and for advice on
blood samples required for further investigation.
38. Management of Mismatched
Blood Transfusion
Investigation:
1. Blood grouping, cross matching of pt. and transfusion bag (donor)
2. S. Electrolytes
3. Blood Urea, S. Creatinine
4. Coagulation status – BT, CT, Platelet count, FDP, Fibrinogen
5. ECG – to see hyperkalaemia
Management of Complication:
1. DIC: Fresh blood, clotting factor, Inj. Hydrocortisone
2. Renal Failure: Treatment of renal failure.
39. Blood Substitute
Def: Are an attractive alternative to costly process of donating, checking, storing
and administrating blood.
Mechanism: Mimic the standard Oxygen carrying capacity of blood.
Advantages:
1) Reduce the immunogenic complication
2) Reduce potential infectious complication
Types:
1) Biomimetic: Haemoglobin based
2) Abiotic: Perfluorocarbon based
Substitute Use
Albumin Severe Hypoalbuminemia
Dextran Hypovolemia, Prevent Thromboembolism
Gelatin Plasma Expander
Hydroxy Ethyl Starches Plasma Expander
40. Stay Safe & Stay Home in this COVID-19 Pandemic