HAEMORRHAGIC SHOCK loss of more than 30-40% blood volume results in fall in blood pressure and gross hypoperfusion of tissues leading to haemorrhagic shock Class IWhen blood loss is less than 750 ml (<15 % of blood volume) 60-70% of blood volume is present in low-pressure venous system(capacitance vessels). 10% of blood volume is present in splanchnic circulation peripheral venoconstrictioncompensates for loss of blood volume by shifting blood into central circulation mild tachycardia and thirst blood pressure, urine output and mentation are all normal Class Il Loss of 800-1500 ml (15-30% of blood volume) Peripheral venoconstriction adrenaline and noradrenaline (catecholamines)released from sympatho- adrenal system cause vasoconstriction of both arteries and veins. Increased secretion of ADH causes retention of water and salt. Thirst increases patient shows heart rate of 100-120 beats/minute and elevated diastolic pressure..Systolic BP normal Urine output is reduced to 0.5 ml/kg/h capillary refill is more than normal 2 seconds Pale extremities... patient is confused and thirsty. Class III Loss of 1500-2000 ml (30-40% of blood volume) patient's systolic and diastolic blood pressures fall, heart rate increases to 120 beats/minute...pulse is thready. respiratory rate increases to more than 20/minute. Urine output drops to 10 to 20 ml/hour. patient appears pale and is aggressive, drowsy orconfused. Class IV blood loss of more than 2000 ml (> 40% of blood volume) peripheries are cold and ashen....pulse is thready and more than 120/ minuteblood pressures are low or unrecordable. There is renal shut down and patient may be moribund. If persistent, can damage other organs, for exampleGIT:, upper GI bleeding, absorption of bacteria andtoxins, bacterial translocation and bacteraemia Liver: Reduced clearance of toxinsKidney: Acute renal failure Heart: Myocardial ischaemia, depressionLungs: Loss of surfactant increased arteriovenous shunting results in acute lunginjury (ALI) result in multiorgan failure associated with high mortality rate. Management Treatment of shock—General measuresHospitalisation Care of all critically ill patients starts with A, B and C. A-Airway, BBreathing and C - Circulation Oxygen administered by facemask for all patients who are in shock but are conscious and are able to maintain their airway If unconscious, endotracheal intubation and ventilation with oxygen Urgent intravenous administration of isotonic saline to restore blood volume to normal. Colloids such as gelatins or hetastarch in Class IV shock or patient is anaemic, blood transfusion is indicated. Investigations: Blood is collected at earliest opportunity for routine investigations Cross-matched blood is given. When life-threatening, uncross matched, O -ve packed cells is transfused into patient Treatment of shock—Specific measures Pressure and packing To control bleeding from nose, scalp: packing using roller gauze with or without adrenaline to control bleeding from nose. Sengstaken tube is used to control bleeding from oesophageal varices internal tamponade. Position and rest..Elevation of leg controls bleeding from varicose veins Elevation of head end reduces venous bleeding in thyroidectomy—Anti- Trendelenberg position. 3.tourniquestsReduction of fractures...Repair of tendons Surgical methods to control haemorrhage:Application of artery forceps (Spencer Well's forceps) to control bleeding from veins, arteries and capillaries. Application of ligatures for bleeding vesselsCauterisation (diathermy) Application of bone wax to control bleeding from cut edges of bones. Silver clips are used to control bleeding from cerebral vessels(Cushing’s clip). Shock is defined as acute clinical syndrome characterised by hypoperfusion and severe dysfunction of vital organs. There is failure of circulatory system to supply blood in sufficient quantities or under sufficient pressure necessary for optimal function of organs vital to survival Classification Hypovolaemic shock..Cardiogenic shock..Distributive shock Obstructive shock Hypovolaemic Shock Loss of blood—haemorrhagic shockLoss of plasma~—as in burns shock Loss of fluid — dehydration as in gastroenteritis HYPOVOLAEMIC SHOCK Decreased preload L Decrease in stroke volume 4 Sympathetic nervous system activation Features primary problem is decrease in preload.decreased preload causes decrease in stroke volume. Severe (Class Illor IV) shock results in tachycardia, low blood pressures and decreased urine output. peripheries are cold and the patient is confused or moribund. Treatment Replace lost blood volumeCrystalloids2-3 times volume of blood lost is replaced with isotonic saline (0.9% saline) or Ringer lactateColloids: 1-1.5 times blood lost is replaced with colloid instead of crystalloid (5% albumin, gelatin or hetastarch) Blood transfusionif large amounts of blood is lost (Hb <8-10 gm%) or if patient is anaemic. Cardiogenic Shock blood flow is reduced because of intrinsic problem in heart muscle or its valves.e.g massive myocardial infarctiondamage cardiac muscle Features primary problem is decrease in contractility of heart. causes decrease in stroke volume sympathetic nervous system is activated systemic vascular resistance increases patient presents with tachycardia, low blood pressures and decreased urine output. jugular venous pulse is raised, a S3 or S4 gallop may be present. lumg fields show bilateral extensive crepitations due topulmonary oedema. peripheries are cold and patient is confused or moribund. Treatment Oxygenation improved by administering oxygen, either byfacemask or by endotracheal intubation and ventilation Inotropes: improve cardiac muscle contractility. Vasodilators nitroglycerine dilate coronary arteries andperipheral vessels to improve tissue perfusion. Intra-aortic balloon pump or ventricular used to help ventricles. If unresponsive, revascularisation or valve replacements is considered on an emergency basis. Distributive Shock occurs when afterload is excessively reduced. Distributive shock can occur in following situations. Septic shock Anaphylactic shock Neurogenic shock Septic Shock Pathophysiology Sepsis is response of host to bacteraemia/endotoxaemia.produced bybacteria, viruses,fungi Severe sepsis can result in persistent hypotension despite adequate fluid resuscitation and is called septic shock Local inflammation and endotoxin, elaborated from organisms activate neutrophils, monocytes, and tissue macrophages. Thisresults in cascade of pro inflammatory and anti-inflammatory cytokines andmediators, such as IL-1, IL-8, IL-10, tumour necrosis factor-alpha, prostaglandin E1, endogenous corticosteroids,and catecholaminescellular Chemotaxis, endothelial injury, and activation of coagulation cascade. Features These substances produce low systemic vascular resistance (peripheral vasodilatation) and ventricular dysfunction resulting in persistent hypotension. Generalised tissue hypoperfusion..cellular dysfunction, lactic acidosis (anaerobic metabolism) and , multi-organ failure. septic shock produce evidence of volume depletion, such as dry mucous membranes, and cool, clammy skin includes tachycardia,bounding pulses with widened pulse pressure, hyperdynamic ..precordium on palpation, and warm extremities. Signs of infection include fever, localized erythema or tenderness, consolidation on chest examination, abdominal tenderness, Signs of end-organ hyoperfusion include tachypnoea, cyanosis, mottling of the skin, digital ischaemia, oliguriaand alteredmental status. Treatment Removal of septic focus e.g. resection of gangrenous bowels, closure of perforation, appendicectomy Supportive care: Oxygenation and if necessary Intravenous fluids:done using crystalloids, colloids and blood Blood transfusions is required to maintain patient's haemoglobin levels to 10 gm% Vasoactive agents such as norepinephrine to produce vasoconstriction and raise systemic vascular resistance to normal. Dopamine, dobutamine or adrenaline to increase myocardial contractility Activated Protein Cprevents release of inflammatory mediators and prevents/deactivates action of mediators on cellular response to inflammationAnaphylactic Shock FeaturesOccurs on exposure to allergen patient is sensitive to. reaction may be in form of mild rashes with or without bronchospasm or patient presents with rashes, generalized oedema including laryngeal oedema, bronchospasm and hypotension and if not treated in time, cardiac arrest. Treatment Primary Oxygen and if necessary Adrenaline, 0.5-1 mg IM or 50-100 yg intravenous bolus Intravenous fluids —isotonic saline or Ringer lactate Leg end elevation of bed. Secondary...Chlorpheniramine maleate Hydrocortisone 100 mg intravenously tryptase levels... If raised, they confirm anaphylactic reaction. Neurogenic Shock Causes High spinal cord injury...Vagolytic shock. Features Hypotension without tachycardia, may deteriorate to produce shock and cardiac arrest. Treatment..Intravenous fluids, inotropes and vagolytics BLOOD TRANSFUSION Indications for Blood Transfusion |. To replace acute and major blood loss as inHaemorrhagic shock Major surgery —open heart surgery, gastrectomy..Extensive burns Il. To treat anaemia due to Chronic blood loss as in haemorrhoids, bleeding disorders, Inadequate production as in malignancies, nutritional anaemia ADVANTAGES OF BLOOD TRANSFUSION + Volume replacement * 10, carrying capacity + Replacement of clotting factorsTo replace platelets in thrombocytopaenia, fresh frozen plasma in vitamin K deficiency unresponsive to vitamin K replacement as in liver disease or to reverse effects of warfarin, cryoprecipitate to replace fibrinogen in patients With disseminated intravascular coagulation Chae) aE) Ns GUIDELINES: WHEN TO TRANSFUSE 1. Blood loss > 20% of blood volume 2. Haemoglobin < 8 g/dl 3. Haemoglobin < 10 g/dl in patients with major cardiovascula disease (e.g. ischaemic heart disease) BLOOD PRODUCTS Packed red blood cells (PRBC): When whole blood is centrifuged, red blood cells settle down and platelet rich plasma remains supernatant. Each bag of packed cells contains 250 300 ml with red cellconcentration of 70% Red cell transfusion is required for patients whose haemoglobin is < 7 g%, as in patients undergoing chemotherapy, major surgery higher transfusion threshold (9-10 g%) used for patients with cardiac disease. Each unit of packed cells should increase haemoglobin by 1 g% and haematocrit by 3% red cells may be leucodepleted for use in patients requiring multiple transfusions to prevent development of antibodies to leukocytes Slow transfusion is indicated in patients with cardiac disease, renal dysfunction, severe chronic anaemia and in paediatric patients Packed red blood cells must be both ABO and Rh compatible unless patient has life-threatening massive bleeding, in which case O -ve packed cells may be transfused. Platelets: bag containing platelet rich plasma is again centrifuged to express off plasma bag with remaining platelets can sealed off. Each unit (50 ml) should contain at least 5.5 x 1010 platelets (platelet concentrate) and each unitshould elevate the platelet count by 5-10,000 cells/ cu mm in a 70 kg person Prophylactic platelet transfusion is done when platelet count is< 10,000 cells/cu mm in oncology patients. Therapeutic platelet transfusion is required in patients whoare known to be thrombocytopaenic and are actively bleedin! (platelet count < 50,000 cells/cu mm) One unit of platelets (60 ml) : every 10 kg body weight. Fresh frozen plasma (FFP): remaining plasma (200-230 ml) may be stored in a frozen format -I 8°C for one year needs to be thawed over half hour before use. Fresh frozen plasma transfusion is indicatecd in patients with prolonged INR > 1.5 and are bleeding require surgery provides coagulation factors to those patients who are actively bleeding and those on warfarin is administered in a dose of 10-20 ml/kg body weight. FFPs must be ABO compatible. Cryoprecipitate: fresh frozen plasma is further treated to produce cryoprecipitate rich in fibrinogen Transfusion is indicated in patients whose fibrinogen levels are < 1 g%, e.g. disseminated intravascular coagulation (DIC). dose is 0.2 units/kg body weight Always obtain informed consent from patients or immediate relatives (in emergent situations) prior to transfusion. + Recheck patient's blood group and of donor blood,patient's hospital number and blood bag number is checked Check date of collection and date of expiry before transfusion. STORAGE OF BLOOD 2 Preservative RBC survival (day: ACD (acid-citrate-dextrose) 24 CPD (citrate-phosphate-dextrose) 28 CPDA (citrate-phosphate-dextrose-adenine) 36 SAGM (saline-adenine-glucose-mannitol) 35 Whole blood transfusion is not advisable for routine use fibrinogen concentrate(high risk of hepatitis), Factor VIII and Factor IXconcentrates(for use in haemophilia and Christmas diseaserespectively) and Factor Vil concentrate (for use tn disseminated intravascular coagulation-DIC COMPLICATIONS OF BLOOD TRANSFUSION |. Immune complications 1. Haemolytic reactions a. Major (ABO) incompatibility reaction result of mismatched blood transfusion causes intravascular haemolysis. Clinical features + Haematuria: Pain in the loins (bilateral)+ Fever with chills and rigors Treatment + Stop the blood. Send it to blood bank and recheck. + Repeat coagulation profile + IV fluids, monitor urine output, check urine for Hb + Diuresis with furosernide 20-40 mg IV b. Minor incompatibility reaction * Occurs due to extravascular haemolysis: mild, occurs at 2-21 days Occurs due to antibodies to minor antigens + Malaise, jaundice and fever: Treatment is supportive 2. Nonhaemolytic reactions a. Febrile reaction Occurs due to sensitisation to WBCs or platelets +Increased temperature-no haemolysis b. Allergic reaction * Occurs due to allergy to plasma products; manifest as chills,rigors and rashes all over antihistaminics such as chlorpheniramine ..maleate 10 mg IV. Massive blood transfusion Definition: Massive blood transfusion variously defined-replacement of> 1 blood volume ( or > 10 units of packed cells) in 24 hours, half patient's blood volume in six hours, > 4 RBC units in one hour with ongoing need for transfusion, 500 ml over 5 min or even blood loss > 150 ml/ min with haemodynamic instability and need for transfusionblood bank is intimated to activate massive transfusion protocoinitial request for 4 units ofO -ve red blood cells! (MTP) Disseminated intravascular coagulation (DICOccurs in massive blood transfusion produces severe afibrinogenemia treated by replacement with fibrinogen ( cryoprecipitateand other clotting factors. (Whole biooa I 1 Packed red cells " Pintle concanata = frozen [[eryerreapnat + Prepared by centtugation of whole {pooled (fina (FP) | Ftoanogen load and removing plasma ood strona Factor vill + Used to correct chronic anaemia topaenia Factor IX + Economical and safe Factor Vil ——____——" Albumin Fig. 12.1: Blood products Wound is a discontinuity or break in surface epithelium Types of wounds 1A. Closed wounds + Contusion: Abrasion: Haematoma Contusion: Can be minor soft tissue injury without break in skin, or major when being run over by vehicle. produces discolouration of skin due to collection of blood underneath. Abrasion:epidermis of skin is scraped away exposing dermispainful as dermal nerve endings are exposed. These wounds need cleaning, antibiotics and proper dressings. Haematoma refers to collection of bloodfollowing injury. It can occur spontaneously in patients who have bleeding tendencies such as haemophilia Depending upon the site, it can be subcutaneous, intramuscular or subperiosteal. Small haematomas get absorbed. B. Open wounds+ Incised- Lacerated + Penetrating: Crushed Incised wounds: They are caused by sharp objects such as knife, blade, glass, etc. wound has sharp edge and is less contaminated Primary suturing is ideal gives neat and clean scar. Lacerated wounds: caused by blunt injury such as fall on a stone or due to road traffic accidents Edges are jagged. The injury may involve only skin and subcutaneous tissue or sometimes deeper structures there is crushing of tissue result in haematoma, bruising or even necrosis of tissue. wounds are treated by wound excision and primary suturing Penetrating wounds:Stab injuries look like an innocent injury with small, 1 or 2.cm long cut but internal organs such as intestines, liver, spleen or mesenteric blood vessels may have been damaged Layer by layer exploration and repair, Crushed or contused wounds:caused by blunt trauma due to run over by vehicle, wall collapse, wounds are dangerousmay cause severe haemorrhage, death of the tissues and crushing of blood vessels patients are more prone for gas gangrene, tetanus, etc treatment involves good debridement and removal of all dead and necrotic tissues es [Gieaning end bandage (Active viceaa a) Stop the bleeding | F I lint, if there is fracture - Ee <3 IV line, resuscitation | Fig. 1.1: Wound managementHealing of the wound Healing by primary intention occurs in clean incised wound such as surgical incision wherein there is potential space between edges. It produces clean, neat, thin scar. Healing by secondary intention refers to wound which is infected, discharging pus or wound with skin loss. Such wounds heal with an ugly scar. COMPONENTS OF WOUND HEALING Platelet-deriv. tatelet | growth factor — (PDGF) A =] tract PMN + Macrophag [Remove devitalised tissues | Fig. 1.2: Inflammatory and proliferative phases Injury results in release of mediators of inflammation,mainly histamine from platelets, mast cells andgranulocyte results in increased capillary permeability. + Later kinins and prostaglandins act and chemotactic role for white cells and fibroblasts. «In first 48 hours, polymorphonuclear (PMN) leukocytesdominate. play role of scavengers by removing dead and necrotic tissue ll. Proliferative phase (collagen phase) + Between 3rd and 5th days, polymorphonuclear leukocytesdimi number but monocytes increase.are specialised scavengers. + By 5th or 6th day, fibroblasts appear, proliferate and give rise to, sh inprotocollagen which is convertedinto collagen in presence of an enzyme, protocollagen hydroxylase. 02, ferrous ions and ascorbic acid Fibroplasia along with capillary budding gives rise to granulation tissue. Secretion of ground substance-mucopolysaccharides byfibroblasts takes place Protooliag enhydroxylase costars hydroxylation = Collagen are called proteoglycans help in binding of collagen fibres teoglycans. They help in binding of collagen fibres. , wound is Fibre +Gel + Fluid system Epithelialisation occurs mainly from edges of wound by process of cell migration and cell multiplication. brought by marginal basal cells. within 48 hours, entire wound is re-epithelialised. Ill. Remodelling phase (maturation)|It starts after 4 days and is completed by 14 days.by specialised fibroblasts called myofibroblasts Wound contraction occurs when there is loose skin as in back and gluteal region. Skin contraction is greatly reduced when it occurs over tibia malleolar surface. Corticosteroids, irradiation, chemotherapydelay wound contraction. Connective tissue formation: Formation of granulation tissue isimpottant and fundamental step in wound healing IV. Phase of scar formation + Fibroplasia and laying of collagen is increased + Vascularity becomes less (devascularisation) + Epithelialisation continues + Ingrowth of lymphatics and nerve fibres takes place + Remodelling of collagen takes place with cicatrisation,resulting in scar. Complications of wound healing 1. Infection: responsible for delay in wound healing. Majority of bacteria are endogenous.RESCREDEY sre hang + Tissue loss + Polymorphonuclear cells (PMN) Macrophages Fibroblasts appear 1 Granulation tissue + Exposure of extracellular matrix to platelets Bridge the transition of inflammatory to proliferative phase + Platelet region + Remove dead and necrotic tissie Phagocytosis + Role of T-lymphocytes is not clear + Wound contraction takes place + Inflammatory mediators + Epithelialisation a ee. ¢ 25g) EB 3S" Fig. 1.3: Platelets Fig. 1.4: Polymorph Fig. 1.5: Macrophage Fig. 1.6: Lymphocytes 2. Ugly scar: It is result of infections3. Keloid and hypertrophic scar 4. Incisional hernia and wound dehiscence5. Pigmentation of the skin 6. Marjolin's ulcer WOUND CLOSURE OR WOUND SUTURING 1. Primary suturing: Suturing wound within few hours following an injury (six hours is ideal) is called primary suturing. incised or cut wound with a sharp object such asknife or razor blade. + Minimal injury to structures on either sid 2. Wound excision and primary suturing of skin indicated when: + Wound edges are jagged. + Wound is contaminated with organisms or foreign body. + Tissues are crushed and devitalised. Precautions to be taken are: + It should be done within 6 hours. + Tetanus and gas gangrene prophylaxis. 3. Wound excision and delayed primary suturing indicated in lacerated wounds with major crush injuries. Wound is irrigated with saline and left open without suturing and dressing is applied. + Wound is re-examined 4-6 days later Wound with skin loss follow surgical procedures or accidents, etc.Principles of debridement + Ideally done under general anaesthesia + Assess the extent of injury/loss of tissues Control bleeding + Excision of devitalised tissue better done with scissors * Good saline wash/irrigation is better than betadine/hydrogen peroxide wash. 4. Secondary suturing: After operation , sutures giveway because of severe infection with persistent discharge of pus. In such cases 7-14 days later, after controlling infection skin is freed from edge of wound and granulation tissue and skin are approximated FACTORS AFFECTING WOUND HEALING General factors 1. Age: In children, wounds heal faster. Healing is delayed inold age. Dermal collagen content decreases with aging. 2. Debilitation results in malnutrition. Wound healing isdelayeZinc deficiency is known to delay healing of pilonidal sinus. d because of vitamin C deficiency 3. In diabetic patients, wound healing is delayed because of microangiopathy, atherosclerosis,decreased phagocytic activity, proliferation of bacteria due to high blood suga Jaundiced and uraemic patients have poor wound healingbecause fibroblastic repair is delayed. 5. Cytotoxic drugs such as doxorubicin and malignancydelay healing CHEMOTHERAPEUTIC DRUGS Decrease mesenchymal cell proliferation Reduce number of platelets Reduce inflammatory cells Reduce growth factors Decrease wound breaking strength 6. Generalised infection: Pus delayswound healing. 7. Corticosteroids given early may delay wound healing because of their anti-inflammatory activity.Local factors 1. Poor blood supply: Wound over the knee and shin of tibiaheals very slowly but wound on face heals fast. 2. Local infection: Organisms eat away suture material, destroy granulation tissue and causes slough and purulent discharge. If bacterial count exceeds 105 organisms/mg tissue or if any hemolytic streptococci are present, wound does not heal. Collagen synthesis is reduced and collagenolysis is increased. 3. Haematoma precipitates infection. 4. Faulty technique of wound closure. 5. Tension while suturing. 6. Hypoxia: Killing property of macrophages and production,of fibroblasts can decrease due to hypoxia Inanaemic patients, wound healing is delayed because ofdecreased angiogenesis and decreased collagen production. + Smoking causes vasoconstriction and elevated carbonmonoxide levels BOIL also called furuncle. It is a hair follicle infectioncaused by Staphylococcus aureus or secondary infectionof sebaceous cyst starts with a painful indurated swelling with surrounding oedema. After about 1-2 days, softening occurs in centreand pustule develops which bursts spontaneouslydischarging pus. Necrosis of subcutaneous tissues produces greenish slough. Skin overlying boil undergoes necrosis Furuncle of external auditory meatus is very painful condition because of rich nerve supply of skin Treatment of boil Incision and drainage with excision of slough. Antibiotic cloxacillin is given. Diabetes, if present, is treated Complications of boil Necrosis of skin Pyaemic abscess and septicaemia. + Cavernous sinus thrombosis due to boil on face or stye on eyelid CARBUNCLE infective gangrene of subcutaneous tissuecaused by Staphylococcus aureus commonly occurs in diabetic patients. Patients with poor immunity, or undergoing radiotherapy + Sites: Nape of the neck is the commonest site followedby back and shoulder regionPathology initial lesion is similar to a boil in form of hair follicle infection with perifolliculiti results in necrosis of subcutaneous fat which gives rise to multiple abscesses abscesses are intercommunicating and they open to exterior by multiple openings which are called sieve-like openings a eS PRECIPITATING FACTORS COMMON LOCATIONS Mao eed + Scratching Face and back of the neck + Diabetes Axilla + Poor immunity Gluteal region FACTS ABOUT A BOIL : On the skin of face Dangerous boil = Tender boil : External auditory + Sweet boil Diabetic patients + Boil likes Oily skin + Blind boil or dull boil Subsides without suppuration This appearance is described as cribriform appearance which is pathognomonic of carbuncle. Clinical features Severe pain and swelling in nape of neck. + Constitutional symptoms such as fever with chills and rigors Surface is red, angry looking like red hot coal. + Surrounding area is indurated. + Later, skin on centre of carbuncle softens and peripheral satellite vesicles appear, which rupture discharging pus andgiving rise to cribriform appearance end result is development of large crateriform ulcer with central slough. Complications 1. Worsening of the diabetic status resulting in diabeticketoacidosis. 2. Extensive necrosis of skin overlying carbuncle 3. Septicaemia, toxaemia. Treatment Diabetes control, with injectable insulin. parenteral antibiotics are given till complete resolution occurs. cloxacillin,flucloxacillin, erythromycin and cephalosporins methicillin-resistant Staphylococcal aureus (MRSA) vancomycin Improve general health of patient. + If carbuncle does not show any softening or if it showsevidence of healing, it is not incised. Surgery is required when there is pus. Cruciate incision is preferred TT SUMMARY OF CARBUNCLE Caused by Cocci Abscesses Communicating Red hot like Coal Appearance Cribritorm, Crateriform ulcer Gangrene Cutaneous (subcutaneous) Drug of choice Cloxacillin Diabetes Contro! Incision Cruciate Coseres cs AMOEBIC LIVER ABSCESS called Tropical abscess ( dysenteric abscess) commonest extraintestinal manifestation of amoebiasis. Aetiopathogenesis disease is caused by Entamoeba histolytica complication of amoebic dysentery can occur in acute stage or in chronic carrier stage. - Infection from caecum (typhlitis) spreads through tributary of superior mesenteric vein. - From sigmoid colon, through tributary of inferiormesenteric vein In right lobe, it is posterosuperior surface whichgets involved because it is extraperitoneal (bare area ofliver). It has no peritoneal covering. + After reaching liverorganism causes destruction of hepatocytes by releasing powerful cytolytic enzymes resulting in liquefaction necrosis. causes aseptic thrombosis of blood vessels resulting in necrosis of livertissue causes anchovy sauce pus, which is chocolate brown in colour, and is mixture of broken down RBCs, hepatocytes,etc. Green pus is refpus is sterileerred to pus mixed with bile Amoebae are rarely present in pus but are present inwall of abscess cavity wall contains monocytes, plasma cells, lymphocytes and fibroblasts. Abscesses are multiple which fuse to form single largeabscess cavity Due to perihepatitis, abscess getsfixed to the diaphragm resulting in immobility of diaphragm. Liver abscess in left lobe gets adhered to anterior abdominal wall amoebic infection of gall bladderand bile does not occur because of deleterious effect ofbile on amoebae. Clinical features Male alcoholics are commonly affected,age groupof 20-40 years. Imore common in men. Seen in patients with low socioeconomic status Severe pain in right hypochondrium is due to enlarged livercalled stage of AmoebicHepatitis low grade fever, weakness, anorexia High grade fever with chills and rigors develop if stageproceeds to pyogenic liver abscess due to secondary bacterial infection of amoebic abscess. + Thoracic symptoms such as nonproductive cough, pleurisyand right shoulder pain Signs + Anaemia, emaciation, toxic look and an earthy complexionis present.* Jaundicepresent if abscesses are multiple, due tocompression of biliary radicles. Liver is enlarged in right hypochondrium, tender andsoft Intercostal tenderness differentiates it from acutecholecystitis Investigations 1. Total WBC count may increase 2. Stool examination for ova and cysts of Entamoeba histolytica may be positive Serologic testing: indirect haemagglutination test ispositive Screening chest:patient is asked to take deep breath, right side of diaphragm does not move due to inflammatory (perihepatitis) adhesions between liver and diaphragm.called homolateral immobility ofdiaphragm. Sigmoidoscopy may demonstrate large, deep amoebiculcers-flask shaped. 6. Abdominal USG: investigation of choice To locate site of abscess and then to confirm diagnosis.+ Ultrasound guided needle aspiration can also be done and biopsy of abscess wall istaken. + Multiple abscesses can be made out. 7. CT scan can demonstrate an abscess cavity as low densityzone surrounded by peripheral hypodense zone due toinflammatory reaction. Treatment Il. US-guided needle aspiration/pigtail catheter drainage amoebic liver abscess Before it is aspirated, bleeding profile (BT, CT, PT) should be normal and injection vitamin K 10 mg, IM given for at least 3 days. + US-guided aspiration is treatment of choice wheremetronidazole is contraindicated, e.g. 1st trimester of pregnancy. Ill. Surgery (open drainage) and laparoscopic Indications 1. Failure of US-guided needle aspiration. 2. Ruptured amoebic liver abscess with amoebic peritonitis Laparotomy is done first. Abscess cavity is identified.Contents are evacuated, a thorough peritoneal wash is given self-retaining Malecot's catheter (any tube drain)is introduced into abscess cavity, brought outside and connected to bag. GAS GANGRENE It is highly fatal, rapidly spreading infection caused b: clostridial organisms which results in myonecrosis Other names Clostridial myositis, clostridial myonecrosis, infective gangrene of muscles. Aetiology caused by Clos Iridium perfringens commonest organism (60%). Other organismismare C/ostridium septicum, Clostridium oedematiens, Clostridiumhistolyticum gram-positive, anaerobic spore-bearing bacilli. Source of infection Manured soil or cultivated soil, normal intestines. Risk group In patients who have had lower limb amputations performed for ischaemic gangrene, infection can occur from patient'sown bowel organisms.+ High velocity gun shot wounds with perforation of hollow viscus are associated with risk of developing gas gangrene (military wound). + Immunocompromised patients are at risk. Pathogenesis develops in wounds where there is heavy contamination with soil or foreign body, or which is associated with laceration and devitalised muscle mass. ess | Predisposing factors for the development of gas gangrene Factors Mechanism Foreign body such as soil, clothing bullets, lass pieces Soil supplies calcium and silicic acid which causes tissue necrosis. Necrosis ofthe tissues results in proliferation ofthe organism, ‘Anoxia due to crushing of the arteries ‘Anaerobic organisms multiply Dead and devialised tissues. Blood cs, Supplies calcium Extravasated haemoglobin and myoglobin Charlee Endogenous infection from patient's faecal matter contamination of a surgical wound such as below knee amputation done Under these favourable conditions clostridial organisms multiply and produce toxins which cause further tissue damage EEE ccs ss few Conran Throwed epes wh aly ot dor ‘apd wenn te pl i Pape cept key Boe 2) se Ste coker ei Law pte fe FECEEEIEY tv andi tects 1k Hysturoaidase + Breaks the cement substance of the muscle cells—hyaluronie acid[rion] Road trafic accident ‘Soi, foreign body, cothing, Ciostidial organisms | Spreading anaerobic clus | [Breakdown of muscle. [Damage tothe ood vessel] ‘muscles change the colour, . |__ tose contactity jemia-Necross-Gan fre {mat tiplication of orgar [Exesive oedema) ofthe nb Production of gas wih spreading infection by the bacteria— | hydrogen sui {Septicsemia and death (H,S), ammonia Fig. 32: Pathological changes Diagnosis examine pus under microscope after staining with Giemsa stain Presence of gas indicates anaerobic metabolism. Prophylaxis 1. Debridement: All dead, necrotic tissue, bone pieces and foreign material are removed. Pus is evacuated. Wound is irrigated with antiseptic agents. 2. Prophylactic antibiotics: Penicillin is drug of choice10-20 lakh units, 4-6thhourly is given for a period of seven days. 3. Judicious and minimal use of tourniquet:4. Gentle but effective application of plaster cast with orwithout treatment of associated fractures to avoidcompression on blood vessel. Treatment of established gas gangrene + Emergency surgery which includes excision of all deadmuscles and necrotic tissues by using generous, longincisions-debridement. + Penicilline Polyvalent anti-gas gangrene serum. + Hyperbaric oxygen TYPES OF GAS INFECTIONS 1. Clostridial cellulitis 2. Local type: It refers to infection confined to a single muscle 3. Group type: It refers to infection confined to one group ofmuscles in compartment. 4. Massive type: Gas gangrene involving entire limb,|s treated by amputation. LUDWIG'S ANGINA refers to cellulitis of submental and submandibular regions combined with inflammatory oedema of mouth. Virulent streptococcal organisms are responsible for infection surrounding submandibular region. PRECIPITATING FACTORS Caries tooth Cancer of the oral cavity Calculi in the submandibular gland Chemotherapy Cachexia Chronic disease—diabetes Observe 6 Cs Clinical features + Elderly patient who presents with diffuse swelling insubmandibular and submental region (Brawny oedema). * Oedema of floor of mouthresult of whichtongue is pushed upwards resulting in difficulty inswallowing. + High grade fever with toxicity.+ Putrid halitosis is characteristic Treatment + Rest and hospitalisation: Appropriate antibiotics + Intravenous fluids to correct dehydration and Ryle’s tube feeding Surgery Under general anaesthesia, 5-6 cm curved incision is made belowmandible in submandibular region over most prominent part of swelling. Submandibular gland is mobilised, mylohyoid muscle is divided and pus is drained..Wound is closed with loose sutures, after irrigating cavity with antiseptic agents and drainage tube is kept in place. Complications |. Mediastinitis and septicaemia 2. Oedema of the glottis due to spread of cellulitis via tunnel occupied by stylohyoid to submucosa of glottis. CANCRUM ORIS «It is extensive ulcerative disease of cheek mucosa occurring in malnourished children. + Precipitating factors are Malnourishment Major diseases such as diphtheria, whooping cough, typhoid, measles and kala azar. opportunistic organisms suchas Vincent's organisms-Borrelia vincentii andB. fusiformis multiply and cause multiple ulcers, erosionsand later, fibrosis. as tdisease progresses, whole thickness of cheek is ost. Treatment of cancrum oris 1. Ryle's tube feeding2. Improve nutrition 3. Appropriate antibiotics: Metronidazole 400 mg three times day for 7-10 days. 4. Reconstructive surgery Complications of cancrum oris |. Fibrosis causing restriction of movement of jaw. 2. Septicaemia, toxaemia and death EPULIS “upon gum". It refers to solid swellingsituated on gumfrom alveolar margin of jaw patients present with swelling on gum whichis painless. Types Granulomatous epulis Precipitating factors are caries tooth, dentures, poor oral hygiene. manifests as mass of granulation tissue aroundteeth on gums.soft to firm, fleshy mass and bleeds on touch. + Pregnancy epulis refers to this variety (gingivitisgravidarum). Fibrous epulis commonest form. fibroma arising from periodontal membrane, presents on gum. firm polypoidal mass, slowly growing and nontender. Giant cell epulis also called myeloid epulis. osteoclastoma arising in jaw presents as hyperaemic vascular, oedematous, soft to firm gums with indurated underlying mass due to expansion of bone. X-ray shows bone destruction with ridging of walls(pseudotrabeculation). Small tumours are treated by curettage. Large tumours are treated by radical excision. Carcinomatous epulis an epithelioma arising from mucous membrane of alveolar margin. presents as nonhealing, painless ulcer. It slowly infiltrates bone. Hard regional lymph nodes are due to metastasis. Treated by wide excision which includes removal ofsegment of bone |. TUBERCULOUS (TB) L YMPHADENITIS Specimen of lymph nodes which are matted. Cut surfaceshows caseation Central caseation surrounded by epithelioid cells, Langhans ' type of giant cells. 3. What are the stages of TB lymphadenitis? + Stage of lymphadenitis: Stage of matting + Stage of cold abscess: Stage of collar stud abscess + Stage of sinus formation Stage of collar stud abscess results when cold abscess which is deep to deep fascia ruptures through deep fascia and forms another swelling in subcutaneous plane which is fluctuant. Cross fluctuation test may be positive treated like cold abscess. collar stud abscess ruptures through skin.lead to stage of sinusSubcutaneous tissue cog abscess Rupture Deep fascia Skin Fig. 2.11: C6ilar Stud) abscess triage is derived from the French word trier, meaning to sort. This is method of sorting out injured patients, duringmass casualties depending on severity of injury Triage is skilled activity by a Trauma team, wherein thereis leader and there are many assistants. leader sorts out patients (people) depending upon their severity of injury. + Each of patients can be colour coded (a coloured flagls attached to them). Examples 1. Immediate help is necessary-Red: Otherwise person will die in few minutes if no treatment is offered,e.g. obstructed airway, tension pneumothorax. 2. Urgent help is necessary- These patients maydie in 1-2 hour if no treatment is given. Examples arecases of massive bleeding and hypovolaemia. 3. Delayed-Green: These patients can wait. Examplesare minor fractures. 4. Expectant-Blue: Very severe injury and unsalvageable. An attempt to treat them, may delay treatment to otherpatients who are salvageable. 5. Dead people are flagged-white or black. Acommon scheme 1. Can the patient walk? Yes-Delayed (green) No-Check for breathing 2. Is the patient breathing? No: Open the airway Are they breathing (ventilating) him? Yes-immediate (red) No DEAD (white)Yes: Count or estimate respiratory rate (over 15 sec). < 10 to> 30 per minute-immediate (red) 10-30 per minute-check the circulation. 3. Check the circulation Pulse >120/min (capillary refill >2 s)-immediate (red) Pulse< 120/min (capillary refill< 2 s) urgent (yellow) Triage algorithm Step One (Assess physiological impact) Measure vital signs and level of consciousness ™ By Glasgow coma scal™ Systolic blood pressure™ Respiratory rate ™ Revised trauma score. It is based on airway, laryngeal injury, spine injury, maxillofacial injury Step Two (Assess anatomical impact) All penetrating injuries to head, neck, thorax, major burns, fracture bones, pelvic fractures, paralysis Step Three (Assess mechanism) Automobile accidents, crash or blast injuries, high energy injuries, fall from more than 20 feet. Bullet injury Step Four (Assess history) ™ Patient's age below 5 years or age more than 55 years ™ Cardiac diseases, respiratory and metabolic diseases ™ Pregnancy ™ Patients with bleeding disorders ™ Immunosuppressed individuals BASED ON THESE STEPS CONSIDER TO SHIFT THE PATIENT TO TRAUMA CENTER and TRAUMA TEAM SHOULD BE KEFATEA ALERT QUICK REMINDER MNEMONIC AT TREATMENT CENTRE ¢ Lift jaw * Intubation: Airway * Fallen tongue/foreign body to be checked * Tracheostomy/cricothyrotomy/oropharyngeal or naso- pharyngeal throat suction ¢ Jaw fractures to be ruled out Glasgow Coma Scale (GCS) is used to objectively describe extent of impaired consciousness in all types of acute medical and traumapatients. scale assesses patients according to three aspects of responsiveness: eye-opening, motor, and verbal responses. Reporting each of separately provides clear, communicable picture of patient... findings in each component of scale can aggregate into total Glasgow Coma Score which gives less detailed description but can provide useful summary of the overall severity. Objectives: Explain the value of Glasgow Coma Scale for patient care. Outline the three areas Glascow Coma Scales assesses. Summarize severity findings for each range of Glascow Coma Scale. was first published in 1974 at University of Glasgowby neuro surgery professors Graham Teasdale and Bryan Jenne Glasgow Coma Scale divides into three parameters: best eye response (E), best verbal response (V) and best motor response (M). levels of response in components of Glasgow Coma Scale are ‘scored’ from 1, for no response, up to normal values of 4 (Eye-opening response) 5 ( Verbal response) and 6 (Motor response) Score thus has values between three and 15, three being the worst and 15 being the highest. score is sum of scores as well as individual elements Best eye response (4) No eye opening Eye opening to pain Eye opening to sound Eyes open spontaneously Best verbal response (5)No verbal response Incomprehensible sounds Inappropriate words Confused Orientated Best motor response (6) No motor response. Abnormal extension to pain Abnormal flexion to painWithdrawal from pain Localizing pain Obeys commands Application of the Glasgow Coma Scale in Pediatrics used in children older than 5 years with no modification. Younger children and infants are not able to provide necessary verbal responses for practitioner to use scale to assess their orientation or obey commands to evaluate their motor response. Children less than 2 years old (pre-verbal) / Children greater than 2 years old (verbal) Best eye response No eye opening / 1 No eye opening Eye opening to pain / 2 Eye opening to pain Eye opening to sound / 3 Eye opening to sound Eyes open spontaneously / 4 Eyes open spontaneously Best verbal response None / 1 None Moans in response to pain / 2 Incomprehensible sounds Cries in response to pain / 3 Incomprehensible words Irritable/cries / 4 Confused Coos and babbles / 5 Orientated - appropriate Best motor response No motor response / 1 No motor response. Abnormal extension to pain / 2 Abnormal extension to pain Abnormal flexion to pain / 3 Abnormal flexion to pain Withdrawal to pain / 4 Withdrawal to pain Withdraws to touch / 5 Localises to pain Moves spontaneously and purposefully / 6 Obeys commands Issues of Concern Pre-existing factors Language barriers Intellectual or neurological deficit..Hearing loss or speech impedimentEffects of current treatment Physical (e.g., intubation): If patient is intubated and unable to speak, they are evaluated only on motor and eye-opening response and suffix T is added to their score to indicate intubation. Pharmacological (e.g., sedation) or paralysis: If possible, the clinician should obtain the score before sedating the patient. + — Effects of other injuries or lesions Orbital/cranial fracture Spinal cord damage Hypoxic-ischemic encephalopathy after cold exposur Clinical Significance Assessment of responsiveness with Glasgow Coma Scale is used to guide early management of patients with head injury or other kind of acute brain injury existence of a continuous, progressive association between increasing mortality after a head injury and decreases in GCS Score from 15 to 3 In both preverbal and verbal pediatric patients, Glasgow Coma Scale is accurate marker for clinically important traumatic brain injury (i.e., injury requiring neurosurgical intervention, intubation for over 24 hours, hospitalization for more than two nights, or causing death