Lecture Notes on Shock - New Mansoura University PDF

Semester 7- level 4-academic year 2024-2025 By Dr/ Saleh Saleh El Balka Lecture of Surgical Oncology 2024  shock Definition: ❖State of inadequate tissue perfusion ⇨ 1. Impaired cellular metabolism. 2. Accumulation...

Semester 7- level 4-academic year 2024-2025 By Dr/ Saleh Saleh El Balka Lecture of Surgical Oncology 2024  shock Definition: ❖State of inadequate tissue perfusion ⇨ 1. Impaired cellular metabolism. 2. Accumulation of waste products. Classification: a) Hypovolemic. b) Septic. c) Cardiogenic. d) Neurogenic. e) Anaphylactic f) Endocrinal  A) Hypovolemic shock Etiology: ↓ blood volume due to: a) Blood loss: as in hemorrhage b)Plasma loss: as in burn, acute pancreatitis and peritonitis. c) Fluid loss: as in sever vomiting and diarrhea. a) Neural factors: 1) ↓ ABP → ↓ in stimulation of arterial baroreceptors in aortic arch & carotid sinus. 2) ↓ CVP →↓ in stimulation of atrial stretch receptors in right atrium. 3) Hypoxia → stimulation of chemoreceptors in aortic & carotid bodies. All these reduce inhibitory discharge on vasomotor center (VMC) → stimulation of VMC & sympathetic nervous system → Leading to a)Constriction of vein → shift blood to heart. b) Constriction of arterioles → ↑ peripheral resistance. c) ↑Rate & strength of cardiac contraction. b) Endocrinal factors: 1)Stimulation of adrenal medulla: → adrenaline & noradrenaline o Adrenaline →↑ heart rate & contractility. o Noradrenaline → V.C →↑ BP. 2) Stimulation of posterior pituitary → vasopressin → -V.C (all over the body except brain & heart) → ↑ BP -Venular constriction → shift blood to heart. -Antidiuretic effect → oliguria. b) Endocrinal factors: 3) Renal ischemia → Renin → angiotensinogen → angiotensin I → Angiotensin II → o Arteriolar V.C. o Venular V.C. o Stimulation of adrenal cortex → aldosterone → Na&H2O retention. 4) ACTH, cortisol, growth hormone and glucagon: Increased. 5) Insulin release is inhibited by adrenaline & noradrenaline. c) Metabolic response: Protein: Catabolism. Carbohydrate: o Glycogenolysis in liver. o Anerobic glycolysis → lactic acid. Fat: lipolysis by catecholamine: free fatty acid. NB: lactic acid + fatty acid = metabolic acidosis. d) Cellular response " the sick cell syndrome " 1) Cell membrane: Na+ in, K+ out. 2) Ribosomes: no protein synthesis. 3) Mitochondrial damage: No ATP formation. 4) Lysosomal rupture: breakdown of cells & release of proteolytic enzymes causing further damage. e) Micro circulatory changes: 1) Compensation phase: o Catecholamine → contraction of precapillary sphincter → ↓ capillary pressure → capillary refilling from interstitial space → ↑ intravascular fluid. 2) Cell distress phase: o Opening of A-V shunts →↑ cell distress → release of histamine & other mediators → contraction of post capillary sphincter → more slowing of capillary flow e) Micro circulatory changes: 3) Decompensation (irreversible) phase: The resulting anoxia & acidosis → relaxation of precapillary sphincter while post capillary sphincter are still contracting as it is accustomed to this acidic media → sludging of RBCs in capillaries → formation of microthrombi. 4) Failure: Finally, the post capillary sphincter relax → passage of microthrombi to circulation → initiate DIC.  shock A) Stage of correctable shock: With adequate replacement of blood volume → vital signs return to normal. B) Stage of irreversible (refractory) shock: If treatment is delayed → irreversible shock due to cellular anoxia → irreversible damage to microcirculation & multiple organ failure.  MOF Multiple organ failure: 1. Heart: ↓myocardial contractility 2. Small intestine: V.C. of splanchnic area → duodenum ischemic gut → stress ulcer in stomach &translocation of bacteria & endotoxins from the lumen. 3. Liver: hepatic dysfunction. 4. Kidney: Adult tubular necrosis. 5. Lung: adult respiratory distress syndrome (ARDs). 6. Hematological: coagulopathy. Clinical picture of hypovolemic shock a) Pulse: Rapid weak (thready). b) BP & Pulse pressure: ↓. c) Temperature: Subnormal (due to ↓metabolism). d) Respiratory rate: tachypnea & air hunger. e) Skin: pale, cold (VC) and clammy with slow capillary refill and collapsed vein. f) UOP: Oliguria. g) Mental status: vary from anxious in the start to drowsy later (but usually remains alert) Investigations& monitoring of hypovolemic shock in ICU: 1.Clinically: Pulse. BP. Temperature. 2.Urinary catheter: Normal urinary output is 0.5 -1.5 ml/kg/h. 3.Measuring of the Central Venous Pressure (CVP): It can be measured by using the usual central venous catheter or better swan Ganz catheter. SVC. - RA & RV - Pulm. trunk - Wedge pulm. Pressure Normal CVP = 5-15 cm water. NB: ↓CVP: hypovolemic shock. ↑CVP: cardiogenic shock. Investigations& monitoring of hypovolemic shock in ICU 4.Blood Chemistry: BI. PH: low (acidosis). Serum electrolytes: ↑serum K+. Blood gases: ↓ PCO2 due to hyperventilation, PO2 is normal. 5.Haemoglobin level & Haematocrite value. 6.ECG.  Treatment I) First Aid Measures 1.Stop external bleeding: by 3 Ps: a) Position→ elevate the bleeding limb. b) Packing of wound. c) Pressure applied by bandage or inflating sphygmomanometer cuff over wound.  First AID.. 2- Resuscitation: A.B.C.D.E A: Airway patency. B: Breathing normally C:Circulation adequate by: 1) Arrest of bleeding. 2) Restoration of blood volume (most important) D: Disability by splinting fractures. E: Exposure of the patient and seek for hidden injury How I could restore the blood volume? By Blood for blood loss, plasma for plasma loss fluid for fluid loss. a) Blood: Advantage: The most effective especially with blood loss. Disadvantages: a) Needs time for grouping. b) May not be available. c) Complications of blood transfusion.  Restoration.. b) Plasma: Advantage: when fresh it supplies the coagulation factors. Disadvantages: a) Expensive. b) Risk of transmission of diseases.  Restoration.. C) Plasma substitutes Dextran: half-life 4 - 24h. Gelatin (Haemagel): half-life 4-5 hours. Disadvantage: a) Haemodilution (not give more than 1 liter) b) Impairs coagulability, and may cause anaphylaxis and nephrotoxicity.  Restoration.. D) Crystalloids 1) Dextrose 5% = 5% glucose → mainly for water replacement 2) Isotonic saline = NaCL 0,9% → for sodium loss 3) Ringer lactate (KCI, NaCl, CaCL2 & Na lactate): For replacement of intestinal fluid loss Advantages: a) Available & cheap b) Decrease blood viscosity so decrease the after load and increase tissue perfusion. Disadvantages: o They escape from the circulation more rapidly.  II. Medications 1) Sedatives: Morphine is ideal → a) Relives pain & anxiety b) Increases the cerebral blood flow It is contraindicated in head trauma or respiratory depression. 2) Corticosteroids Commonly used to combat stress and they have Na & water retention effect.  II. Medications 3) Vasoactive drugs: a) Vasoconstrictors: e.g. adrenaline although they raise blood pressure yet they: 1. Impair tissue perfusion and aggravate tissue hypoxia. 2. Increase the after load on the myocardium. So, they should not be used. b) Vasodilators: e.g. di-phenoxy-benzamine only after good fluid replacement & improving myocardial contractility, they are given to: 1. Improve tissue perfusion. 2. Decrease the after load and heart work  II. Medications 4) Inotropic drugs: e.g. dopamine, dobutamine: to improve myocardial contractility & renal perfusion (dopamine). 5) Antibiotics: e.g. 3rd gen. cephalosporines: to avoid septic complications. N.B. all medications should be given I.V. not I.M or S.C as these last routes are impaired during shock (peripheral V.C.) and if shock is corrected, rapid absorption of repeated injections may cause toxicity.  II. Medications III.Other measures: 1) Position: Elevate the lower limbs about 30 degrees to help venous return from them and improve flow to other vital organs (e.g. brain). 2) Heating: Cover the patient with ordinary blankets. Avoid artificial heating as it increases tissue demands of oxygen.  B) Septic Shock Definition: ❖sepsis + hypotension with systolic < 90 mmHg or drop in BP of > 40 mmHg that is refractory to fluid replacement. Predisposing factors: 1) Extreme of age. 2)DM. 3)Malnutrition. 4)Malignancy 5)Uremia. 6) Patients under corticosteroid or immunosuppressive drugs.  Septic Shock Etiology: ❖It is caused by septicemia especially Gram-ve septicemia. The endotoxin, which is a component of the cell wall of Gm-ve bacteria, released from dead bacteria is responsible for all pathology effects in septic shock.  Septic Shock ❖Surgical causes of septic shock: 1) Sepsis following operation on genitourinary, hepato-biliary & intestinal tracts especially in emergency. 2)Major trauma & burns + sepsis. 3)Transplant patients + sepsis. 4) Septic peritonitis. ❖Non-surgical causes e.g. pneumonia – meningitis.  Pathology ❖The circulating endotoxin stimulates macrophages & kupffer cells of liver to release cytokines (TNF, interleukins, platelet activating factor, PGs & nitric acid) that have a toxic effect on: Microcirculation: 1) Paralysis of the capillary sphincters with pooling of blood in the microcirculation. 2) Disseminated intravascular coagulation. 3) Damage of vascular endothelium → oedema. Cells Cellular hypoxia & anerobic metabolism → lactic acidosis.  Pathology Direct toxic effect on: 1) Heart. 2) Lung→ ARDS. 3) Brain → cerebral ischemia. 4) Kidney → Renal failure. 5) Liver → Cholestasis & jaundice. 6)GIT: o Gastroduodenal stress ulceration + damage of barrier action of the intestinal mucosa leading to more mobilization of intestinal bacteria & endotoxin to the circulation.  causes of death Complications = causes of death: 1. Adult respiratory distress syndrome (ARDS) 2. Multiple organ failure. 3. Acute erosive gastritis. 4. DIC.  Clinical picture ❖The patient passes through two stages: 1-Hyperdynamic (warm) stage: 1) The patient is flushed, feverish (38°C) with warm dry skin. 2) Tachycardia, tachypnoea & hypotension. 3) Restlessness & confusion. 4)Normal or high cardiac output (C.O.P). 5) If not promptly treated, it will pass to the following stage.  Clinical picture 2-Hypodynamic cold stage 1) Cold clammy skin 2) Tachycardia, tachypnea & severe hypotension. 3) Generalized capillary damage. 4) Low cardiac output. 5) It ends with multiple organ failure, DIC & death.  Investigations a) CBC: Leucocytosis & high lactate level. b)Monitoring: as in hypovolemic shock e.g CVP or swan Ganz catheter. c) Looking for a source of sepsis → X ray chest & abdomen, abdominal US, CT scan.. etc. d)Blood culture at the peak of fever or culture from septic focus will guide antibiotic treatment.  Treatment ❖Should be carried on intensive care unit (ICU). ❖TTT has 2 goals→ a) Support body systems. b) Fighting infection. ❖Both should go hand in hand. ❖In addition, monitoring is essential for guidance of ttt.  1)Fighting infection Eradication of sepsis: e.g. Drainage of huge abscess or peritonitis or resection of gangrenous bowel. Antibiotics: Aggressive combinations of broad-spectrum antibiotics should be started immediately (e.g. 3rd or 4th generation cephalosporin + metronidazole) until the results of culture is available.  2)Support different systems Cardiovascular support: The aim is to achieve a CVP of 10-12 cm H2O. a) Fluid replacement: by Ringer lactate. b) RBCs deficiency: is corrected by packed RBCs. c) Medications: 1) Inotropes→ dopamine drip (or a combination of dopamine & dobutamine). 2) Vasopressors→ o If no response & patient remain on hypotensive side. o Careful noradrenaline administration may be given.  1)Support different systems Respiratory support: O2 mask or endotracheal intubation & mechanical ventilation. Renal support: 1) Adequate volume replacement & dopamine administration. 2) Hemodialysis is required in case of acute renal failure, until kidney recover.  3)Monitoring Goes along the same line as hypovolemic shock. Prognosis: ❖Mortality ranges from 25 to 90 %.  C) Cardiogenic Shock Etiology: Due to ↓↓ COP despite a normal VR i.e. pump failure as a result of: a) MI. b) Cardiac tamponade. c) Arrythmia. d) Pulmonary embolism. e) As a complication of any other type of shock.  C) Cardiogenic Shock C/P 1) Low cop symptoms. 2) Congested neck veins. 3) High CVP. TTT Directed to the cause (as ttt of HF in medicine): 1. Potent analgesics must be given to relieve pain in patients with MI. 2. Oxygen 3. Inotropic drugs. 4. Vasodilators to ↑ COP and ↓ myocardial work.  D) Neurogenic shock Mechanism: ❖ Paralysis of vasomotor fibers → widespread VD → peripheral pooling of blood →↓↓ VR. Types: 1. Vaso vagal shock: Etiology Vasomotor paralysis occurs in response to: a) Severe pain (blow to testis or larynx). b) Excitement (hearing bad news or seeing unpleasant event). Pathophysiology This results in: 1. Extensive VD in the splanchnic area → splanchnic pooling of blood → ↓in VR →↓COP→↓in blood supply of vital centers. 2. Excessive vagal stimulation of the heart→ bradycardia. C/P & ttt of vasovagal shock Following a period of anxiety & signs of epinephrine release (tachycardia, tremors, sweating and pallor)→ sudden reflex vagal stimulation → ↓COP & VR → hypotension, bradycardia & syncope (↓CBF). TTT: 1) 1st aid is trendlenberg position. 2)No need for fluid, just remove the patient from the stimulus or relieve the pain if present.  2. Spinal shock Etiology: Due to sympathetic block of the lower half of the body as a result of spinal anesthesia. o This leads to VD of arterioles & venules i.e. pooling of blood in one half of the body with ↓VR. TTT: 1) 1st aid is trendlenberg position. 2) Position + Fluids + Atropine or ephedrine.  E) Anaphylactic shock Etiology: May follow administration of an antigen like antibiotic especially penicillin, anesthetics → release of large amounts of histamine. C/P: 1) Bronchospasm, laryngeal edema and respiratory distress. 2) Hypotension: occurs with massive VD. TTT: 1) 1st aid is trendlenberg position. 2) IV fluids 3) IV corticosteroids. 4) Antihistaminic. 5) ETT may be needed  F) Endocrinal Shock Etiology: 1) Patients with addison's disease. 2) Patients receiving continuous cortisone therapy if they are subjected to any stressful stimulation e.g. infection or surgery. C/P (3H): Hypotension – Hyponatremia – Hyperkalemia. TTT: 1) Prophylactic: Give an additional dose of hydrocortisone before surgery. 2) Established cases: give the patient: 1. Large dose of IV hydrocortisone. 2. Saline infusion. 3. TTT of the predisposing factor e.g. infection.  Surgical Hemostasis *Definition: The mechanism by which the body attempts to stop bleeding after injury or cutting of a blood vessel. * Physiology: [A] 1ry Hemostasis : (1) Vasoconstriction of disturbed vessels. (2) Platelets plug formation. (3) Tamponade of bleeding by surrounding tissue tension.  Surgical Hemostasis [B] 2ry Hemostasis : coagulation is activated by 2 mechanisms * Causes of bleeding during or after surgery: 1)Inadequate Surgical Hemostasis. 2) Defects of Hemostasis.  Defects of Hemostasis [A] Congenital Disorders: Hemophilia A and B These are due to deficiency of factors VIII and IX respectively. Hamophilia A is the most common congenital coagulopathy. Inheritance (in both) is sex linked (from females to males). Management Infusion of factor concentrates within 1 hour before surgery and for 10 days thereafter.  Defects of Hemostasis [B] Acquired Disorders: These are more common than congenital ones: (1) Hepatic disorders. (2) Vitamin K deficiency. (3) DIC (4) Anticoagulants. (5) Massive blood transfusion. (6) Platelets disorders  1) Hepatic Disorders Aetiology: Coagulation factors deficiency: Decreased concentration of all clotting factors except factor VIII (synthesized in other organs). Dysfibrinogenaemia : defective polymerization of the fibrin clot. Platelets deficiency: Thrombocytopenia from splenic sequestration due to hypersplenism. Among patients with cirrhosis, 40% had an abnormal bleeding time >10 minutes (normal bleeding time run in the range of 2-9 minutes). Hyperfibrinolysis.  1) Hepatic Disorders *Treatment: 1)Vitamin K administration. 2)Fresh frozen plasma (2-3 units) replaces the missing coagulation factors. 3)Desmopressin (synthetic analog of vasopressin (ADH)) : antidiuretic plus fewer pressor effect so it may be used for treatment of mild classic hemophilia and von Willebrand's disease. 4) Tranexamic acid (e.g cyklokapron) or other fibrinolysis inhibitors: may be useful in upper GIT haemorrhage.  (2) Vitamin K Deficiency * Aetiology: 1) Lake of vitamin K in diet: a very low fat diet because vitamin K is best absorbed when eaten with some fat. 2) In debilitated patients given prolonged broad spectrum antibiotics (reduce colonic bacteria). 3) Cholestatic jaundice. 4) Fat malabsorption: may occur in people with celiac disease, cystic fibrosis disorders in intestine e.g large part of their intestine removed. 5) Oral anticoagulants. * Function: Vitamin K is a co-factor in the synthesis of factor II, VII, IX, and X.  (2) Vitamin K Deficiency * Investigation: Both the prothrombin time (PT) and partial thromboplastin time(PTT) are prolonged Fibrinogen level and platelet count are normal. * Treatment: ✓ Vitamin K by slow IV infusion (5-10mg) or IM. ✓ In emergency, factor concentrates (II, VII, IX and X) may be given. ✓ Fresh frozen plasma may be needed as well as blood. (3) Disseminated Intravascular Coagulation (DIC) * Aetiology: 1) Septicemia. 2) Severe shock, trauma, and burns. 3) ABO incompatible transfusion. 4) Malignancies, especially metastatic carcinoma of the lung, pancreas, prostate, and leukemia. 5) Obsteteric accidents (eclampsia, amniotic fluid embolism, and retained dead fetus). * Diagnosis is suspected by: 1) Diffuse bleeding from wounds, incisions, drain and venipuncture sites. 2) Widespread bruising, purpura and mucosal bleeding. 3) Occasionally, the thrombi are not lysed quickly and ischemic manifestations occur, e.g. gangrene of skin and digits.  (DIC) * Investigation: 1)Thrombocytopenia 2) High Fibrin degradation product (FDP). 3)Prolongation of PT, PTT and low fibrinogen level (N = 2 - 4g/L). * Treatment: Treatment of the underlying cause to stop the cycles of coagulation/fibrinolysis, e.g. draining an abscess and antibiotics for infection. Replacement of consumed coagulation factors and platelets with fresh frozen plasma and platelet transfusion. Blood transfusion to restore circulating blood volume and oxygen carrying capacity since hypoxia exacerbates DIC. Heparin to stop the thrombotic component may be advocated.  4)Platelets Disorders [A] Thrombocytopenia: Essential thrombocytopenic purpura. Secondary thrombocytopenic purpura may occur secondary to drugs as thiazides, methyl dopa and sulfa drugs, chemotherapy or radiotherapy. [B] Disorders of platelets functions Drugs as aspirin and NSAID inhibit cyclooxygenase and prostaglandin synthesis, thus they interfere with platelet adhesiveness. Cephalosporins and semisynthetic penicillins coat platelets. Dipyridamole (Persantine) reduces platelet adhesiveness. Uremia and hypothermia can cause platelet dysfunction.  Others (4) Anti-Coagulants therapy Can cause bleeding if the dose is not properly adjusted. (5) Massive Blood Transfusion with stored blood  Pre-operative Evaluation of Haemostasis [A] History: (1) Personal History: age: e.g. childhood (Hereditary disorder). (2) Present History: history of abnormal bleeding from multiple sites e.g. epistaxis, bleeding gingiva, petechiae, ecchymosis, haematoma. (3) Past History: history of liver disease, chronic renal failure, massive blood transfusion & drug intake. (4) Family History: suggests Haemophilia (A or B).  Pre-operative Evaluation of Haemostasis [B] Examination: 1. Cutaneous signs of liver disease e.g. jaundice, and spider naevi. 2. Skin and mucous membranes are examined for bleeding, 3. Musculoskeletal system: muscle Haematomas & Hemarthrosis. 4. Abdomen: Hepatomegaly & Splenomegaly. 5. Lymph node enlargement may be caused by lymphoma, chronic lymphocytic leukaemia & IMN.  C Tests of Haemostasis Indications: 1. Patients with personal or Family history of abnormal bleeding. 2. Patients with diseases or who receive medications that can interfere with haemostasis.  C Tests of Haemostasis ∎ Tests for Primary Haemostasis : (1) Platelet Count: Normal =150.000- 400.000/ul. Spontaneous bleeding occurs with counts 10.000-20.000/ul. No hemastatic abnormality occurs in counts more than 100.000/ul. (2) Bleeding Time (BT): is prolonged (n 2-9 minutes) with platelet and vascular defects. (3) Tests of platelet function (adhesion and aggregation). (4) Von Willebrand factor (vWF) and factor VIII assay:  C Tests of Haemostasis VEF is a protein that serves to attach platelets to blood vessel wall and to each other during 1ry hemostasis. Factor VIII is involved in another inherited clotting disorder called hemophilia. But unlike hemophilia, which mainly affect males, von Willebrand disease affect males and females and is usually milder. NB: VWF disease is usually inherited as autosomal dominant disorder, which means you need a mutated gene from only one parent to get the disease. If you have the gene for von Willebrand disease, you have a 50% chance of transmitting this gene to your children. The most severe form of this condition is autosomal recessive which means both of your parents have to pass a mutated gene to you.  C Tests of Haemostasis ∎ Tests of secondary Haemastasis : (1) Prothrombin Time and international normalized ratio (PT/INR): PT measures the time of clotting though the extrinsic and common pathways which involve factor VII & Factors X, V, II and fibrinogen respectively. PT is usually range from 11 to 13.5 seconds. INR (patient PT/Control PT) is usually range from 0.8 to 1.2 and is always used to monitor a patient on warfarin therapy. (2) activated Partial Thromboplastin Time (aPTT) normal value is 30-40 seconds. It measures the time of clotting through the intrinsic and common pathway i.e. assesses factors XII, XI, X, IX, and VIII.  C Tests of Haemostasis NOTES: A prolonged PT and normal APTT indicate a defect in the extrinsic pathway only. Tissue factor is never deficient, so this is diagnostic for factor VII deficiency. A normal PT and prolonged APTT indicate a defect in intrinsic pathway only. this is could be due to deficiencies in prekallikrein, factor XII ,XI,IX,VIII or combinations. A prolonged PT and APTT indicate a defect in common pathway or multiple defect in both pathways.  C Tests of Haemostasis (3) Other Tests Fibrinogen level is decreased in DIC. Fibrin degradation product (FDP) screens for fibrinolysis. Individual coagulation factor essays. Clot stability test evaluates factor XIII, deficiency of which is not detected by (PT) or (aPTT). Clotting time (in vitro tube method): normal range is 4 to 10 minutes.