1.PREPARED BY: MICAH Q. VANDERLIPE 1 LORMA COLLEGES GRADUATE SCHOOL Carlatan, San Fernando City, La Union

2. 2 3. Clinical syndrome caused by accumulation of fluid pericardial space. Resulting in ventricular filling and subsequent hemodynamic compromise. 3 4. Pericardium- membrane surrounding the heart. - composed of two layers. - thicker parietal pericardium =outer fibrous layer. - thinner visceral pericardium =inner serous layer. Pericardial space normally contain 20-50 mL of fluid. 4 5. 3 Phases of Hemodynamic Changes in Tamponade by Reddy et. al., Phase I- Accumulation of pericardial fluid causes in stiffness of the ventricles, requiring a filling pressure. L and R ventricular filling pressure are > intra-pericardial pressure. Phase II- Further fluid accumulation, pericardial pressure above ventricular filling pressure, resulting to CO. Phase III- Further in CO due to the equilibrium of pericardial and L ventricular filling pressures. 5 6. Pericardial Effusion- causes cardiac tamponade can be (a.) serous (b.) serosangeinous (c.)hemorrhagic (d.) chylous. The underlying process for the tamponade development is marked by: 6 Results when transmural distending pressures becomes insufficient to increase intra- pericardial pressures. Reduction in diastolic filling 7. Systemic venous return is also altered during tamponade. 7 Decrease venous return or altered Compression of heart throughout cardiac cycle Increase intra-pericardial pressure, systemic venous return is impaired and R atrial and R ventricular collapse occur Due to Because of 8. Physical Examination Common Symptoms- dyspnea, tachycardia, jugular venous pressure, diminished heart sound, friction rub, dizziness, drowsiness, palpitation, col d clammy skin, weak pulse due to hypotension. Becks Triad- 8 Increase jugular venous pressure, Hypo tension, Dimin ished heart sound Rapid accumulat ion of pericadial fluid. Acute Cardiac Tampona de 9. Pulsus Paradoxus- is an exaggeration of the normal inspiratory decrease in sytemic blood pressure. (>12 mm Hg or 9%). - difference between the 1st and 2nd measurement is > 12 mm Hg, an abnormal pulsus paradoxus is +. -semirecumbent position. -with the use of BP cuff which inflated at least 20 mm Hg above the systolic pressure. 9 10. Kussmauls Sign- Increase venous distension and pressure during inspiration. Ewart Sign- + in patient with large pericardial effusion. - area of dullness with bronchial breath sound and bronchophony below the L scapula. Y Descent- abolished in the jugular venous or right atrial waveform. - increase in intra-pericardial pressure preventing diastolic filling of the ventricles 10 11. Dysphoria- behavioural traits such as restless, unusual facial expression, sense of impending death. Low-pressure Tamponade- tachycardia, pulsus paradoxus, jugular vein distension. 11 12. Imaging Studies Chest Radiography CT scanning- earlier marker for cardiac tamponade Echocardiography Pulse Oxymeter Swan-Ganz Catherization 12 13. Lab Studies Creatine kinase and isoenzymes- increase in MI and cardiac trauma CBC Coagulation panel- bleeding risk during intervention. HIV-testing- pericardial effusion PPD-testing- Dx tuberculosis that causes effusion and tamponade. 13 14. Surgical Care Biopsy Periardiocentesis and Pericardiotomy- definitive therapy. Emergency subxiphoid percutaneous drainage. Echocarrdiographically guided pericardiocentesis. Percutaneous balloon pericardiotomy. Surg. Care in Hemodynamically unstable pt. Surg. Creation of pericardial window. Recurrent cardiac tamponade/pericadial effusion Video-assisted Thorascopic Procedure- feasible treatment. 14 15. Medication Dobutamin- is a synthetic catecholamine and direct inotropic agent that stimulates cardiac beta-receptors with minimal increase in systemic vascular resistance. - increases stroke volume and cardiac output. 15 16. Approaches Oxygen Volume expansion Bed rest with leg elevation Inotropic drugs 16 17. 17 18. Characterized by systemic activation of blood coagulation. Results in generation and deposition of fibrin. Leading to microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome. Derangement of the fibrinolytic system further contributes to intravascular clot formation. 18 19. Pathophysiology Thrombin Generation and Tissue Factor 19 Endothelial disruption, tissue damage inflammation tumour cell Activates coagulation via Extrinsic pathway involving F VIIa Occurs via Thrombin Activates Fibrinogen to fibrin Cleaves Simultaneously causing platelet aggregation 20. TF = expressed in mononuclear cells in vitro and on circulating monocytes of pt with severe infection and may be on endothelial cell when injured, it release TF. 20 Amplify both clotting and inflammation -platelet activation = enhancing aggregation and coagulation -activation of VIII,V,XI = yielding thrombin generation -activation of pro-inflammation factor XIIIa = augment fibrin clots -activation of thrombin-activatable fibrinolysis inhibitor = clots becomes resistant to fibrinolysis -enhanced expression of adhesion molecule = promoting inflammation effects of WBC 21. Impaired Coagulation Inhibitor Systems 21 Antithrombin is continuously consumed by ongoing activation of coagulation Elastase produced by activated neutrophils worsen antithrombin as well as other proteinFurther antithrombin is lost to capillary leakage Production of antithrombin is impaired 2 to liver damage resulting from under perfussion and microvascular cagulation 22. Defective Fibrinolysis 22 Fibrin Thrombin Produced by Process fibrinolysis Eliminated by Rapid fibrinolysis ff. by Suppression fibrinolysis activity Release of plasminogen activators from endothelial cells Caused by Sustained increase in plasma levels of PAI-1 TNF-2 and IL-1 Mediated by High PAI-1 levels DIC 23. Inflammatory Activation 23 Rise in clotting cascade Coagulation stimulates more vigorous inflammation Activated coagulation factor Propagation of inflammation Contribute to Stimulating endothelial cells by Pro-inflammation cytokines Release of 24. Physical Examination PARTS SIGNS Circulatory Life threatening hemorrhage, Subacute bleeding, Diffuse or localized thrombosis Bleeding into serous cavity Central Nervous System Altered consciousness or stupor, Transient focal or neurologic deficits Cardiovascular Hypotension, tachycardia, circulatory collapse Respiratory Pleural friction rub, ARDS GI Hematemesis, hematochezia GU Azotemia, acidosis, hematuria, oliguria, metrorrhagia, uterine hemorrhage Derma Petechiae, Jaundice, Purpura, Hemorrhagic bullae, acral cyanosis, skin necrosis of lower limbs, infarction, gangrene, thrombosis, bleeding24 25. Complications Death Acute renal failure Changes in mental status Respiratory dysfunction Hepatic dysfunction Thrombosis and haemorrhage Cardiac tamponade Hemothorax Intracerebral hematoma Gangrene and loss of digits Shock 25 26. Laboratory Studies Platelet count- A decreasing trend in plt count or grossly reduced absolute plt count is a sensitive indicator of DIC. Clotting time and coagulation factor- are typically prolonged. Test for fibrinogen and FDPs D-dimer- better test for DIC. 26 27. Medication Anti coagulant, Hematologic Heparin Antithrombin (Atryn, Thrombate III) Recombinant Human Activated Protein C Blood Components PRBC; washed Platelet FFP Cryoprecipitate and fibrinogen concentrates Antifibrinolytic Agents Aminocaproic acid Tranexamic acid 27 28. Approaches Monitor v/s Assess and document extent of haemorrhage and thrombosis Correct hypovolemia Administer hemostatic procedure when indicated Administer meds as prescribed 28 29. 29 30. In 1914, Schottmueller wrote Septicimia is a state of microbial invasion from a portal of entry into the blood stream which causes sign of illness. Classification of Shock 1. Hypovolemic 2. Obstructive 3. Distributive 4. Cardiogenic 30 31. SIRS is a term that was developed in an attempt to describe the clinical manifestations that result from the systemic response to infection. 31 Criteria for SIRS: Temperature greater than 38C (100.4F) or less than 36C (96.8F) Heart rate greater than 90 beats per minute Respiratory rate greater than 20 bpm or arterial dioxide tension lower than 32mm Hg WBC count higher than 12000 or lower than 4000 or 10% immature forms. 32. 32 With sepsis, atleast 1 of the following manifestations of inadequate organ function/perfusion is typically included: Alteration in mental state Hypoxemia Elevated plasma lactate level Oliguria 33. Pathophysiology Mediator Induced Cellular Injury 33 Activation of innate immunity called cytokies Activates the coagulation pathways Resulting to Capillary microthrombi and end-organ ischemia 34. Abnormalities of Coagulation and Fibrinolysis 34 Imbalance in hemeostatic mechanism Disseminated intravascular coagulopathy Causing organ dysfunction and death Inflammation mediators instigate direct injury to the vascular endothelium Endothelial cells releases tissue factor Triggering the extrinsic coagulation cascade Accelerating production of thrombin Which converts soluble fibrinogen to fibrin Insoluble fibrin with aggregated plt forms intravascular clots 35. 35 Binding of factor XII to subendothelial surface Process initiated via Activates F XII,XI, X Activated by complex F IX, VIII, calcium, and phospholipids Inflammation cytokines initiate coagulation by avtivating TF 36. Circulatory Abnormalities Potassium- ATP channel directly activated by lactic acid. NO- activates potassium channel 36 Potassium efflux from cell Results to Hyperpolarization inhibition of calcium influx and vascular smooth muscle relaxation Diminished peripheral arterial vascular tone may result in dependency of blood pressure on CO Resulting to Causing vasodilatation Hypotension and shock if insufficiently compensated by increase CO. 37. Mechanism of Organ Dysfunction Autodestructive process that permits the extension of the normal pathophysiologic response to infection, resulting to multiple organ dysfunction syndrome. Organ dysfunction or organ failure may be the first clinical sign of sepsis. MODS is associated with widespread endothelial and parenchymal cell injury because of the ff. proposed mechanisms: 1. Hypoxic hypoxia 2. Direct cytotoxicity 3. Apoptosis 4. Immunosuppression 5. Coagulopathy 37 38. Cardiovascular Dysfunction Significant derangement in the auto- regulation of the circulatory system is typical in patients with sepsis. NO plays a central role in the vasodilatation of septic shock. Impaired secretion of vasopressin also may occur, which may permit the persistence of vasodilatation. Sepsis interferes with the normal distribution of systemic blood flow to organ systems; therefore core organs may not receive appropriate oxygen delivery. 38 39. Pulmonary Dysfunction The pathogens of sepsis-induced ARDS is pulmonary manifestation of SIRS. A complex interaction between humoral and cellular mediators, inflammatory cytokines and chemokines, is involved in this process. A direct or indirect injury to the endothelial and epithelial cells of the lung increases alveolar capillary permeability, causing ensuing alveolar edema. 39 40. 40 Gastrointestinal Dysfunction GI tract may help to propagate the injury of sepsis. Overgrowth of bacteria in the upper GI tract may aspirate into the lungs and produce nosocomial pneumonia. The guts normal barrier function may be affected , thereby allowing transaction of bacteria and endotoxin into the systemic circulation and extending the septic response. 41. Hepatic Dysfunction The abnormal synthetic functions caused by liver dysfunction can contribute to both the initiation and progression of sepsis. The reticuloendothelial system of the liver acts as a first line of defence in clearing bacteria and their products; liver dysfunction leads to a spill over of these products into the systemic circulation. 41 42. Risk factors Extreme age Primary dse. Immunosupression Major surgery, trauma, burns Invasive procedures Previous antibiotic treatment Prolonged hospitalization Childbirth Abortion Malnutrition 42 43. In septic shock, it is important too identify any potential source of infection. The following physical signs help to localized the source of an infection. 43 PARTS SIGNS CNS Infection Profound depression, signs of meningitis Head and Neck Infection Inflamed or swollen tympanic membranes, sinus tenderness, nasal congestion or exudates, pharyngeal erythema and exudates, inspiratory stridor, cervical lymphadenopzthy Chest and Pulmonary Infection Dullness on percussion, bronchial breath sounds, localized rales, any evidence of consolidation Cardiac Infection Any new murmur, especially in patients with a history of intravenous drug use Abdominal and GI Infections Abdominal distension, localized tenderness, guarding or rebound tenderness, rectal tenderness or swelling 44. Pelvic and Genitourinary infection Costovertibral angle tenderness, pelvic tenderness, pain on cervical motion, adnexal tenderness or masses, cervical discharge Bone and Soft Tissue Infections Focal erythema, edema, tenderness, crepitus in necrotizing infections, fluctuance, pain with joint range of motion, joint effusion and associated warmth/erythema Skin Infection Petechiae, purpura, erythema, ulceration, bullous formation, fluctuance 44 45. Complication ARDS- major complication of severe sepsis and septic shock. Acute renal failure DIC Chronic renal dysfunction MI Liver failure 45 46. Laboratory CBC- WBC, hemoglobin, platelets Blood Chemistry- serum electrolytes, sodium, chloride, glucose, serum lactate, Liver function test Coagulation Studies- aPTT and PT Blood Culture Urinalysis and Urine Culture Gram Stain and Culture of Secretions and Tissue Radiography Ultrasonography Computed tomography Lumbar puncture 46 47. Approaches 3 major goals 1. Resuscitate the patient from septic shock using supportive measures to correct hypoxia, hypotension, and impaired tissue oxygenation. 2. Identify the source of infection and treat with antimicrobial therapy, surgery or both. 3. Maintain adequate organ system function guided by cardiovascular monitoring and interrupt the pathogenesis of multiple organ dysfunction syndromes. 47 48. Management Early recognition Early and adequate antibiotic therapy Source control Early hemodynamic resuscitation and continued support Corticosteroids Drotrecognin alpha Tight glycemic control Proper ventilator management with low tidal volume in patients with acute respiratory distress syndrome 48 49. Treatment Respiratory support Circulatory support Antimicrobial therapy Temperature control Metabolic support Correction of anemia and coagulopathy Management of renal dysfunction Nutritional Support 49 50. Medications Vassopressor Norepinephrine Dopamine Dobutamine Epinephrine Vassopressin Phenylephrine Isotonic Crystalloids NSS LR Colloids Albumin Antibiotics Corticosteroids Human Activated Protein C 50 51. 51 52. Obstruction of blood flow through the SVC. Medical emergency and most often manifests in patients with malignant dse process within the thorax. 52 53. Pathophysiology Obstruction of the SVC may caused by neoplastic invasion of the venous wall associated with intravascular thrombosis or more simply, by extrinsic pressure of a tumor mass against the relatively fixed- thin walled SVC. 53 54. Physical Findings Venous distension of the neck and chest wall, facial edema, upper extremities edema, mental changes, plethora, cyanosis, papilledema, stupor, and even coma. Bleeding forward or lying down may aggravate the symptoms and signs 54 55. Imaging Studies Chest radiography CT scan MRI Invasive contrast venography Radionuclide technetium-99m venography Gallium single-proton emission CT scanning 55 56. Surgical Care Surgical bypass Stenting 56 57. Medications Corticosteriods- dexamethasone Thrombolitics- urokinase Anticoagulants- heparin/warfarin 57 58. 58 59. Hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume, which results in impaired water excretion. 59 60. Pathophysiology The key to understanding the pathophy, signs, symptoms and treatment of SIADH is the awareness that the hyponatremia in this syndrome is a result of an excess of water and not a deficiency of Na+. 60 61. Signs and Symptoms 61 Depending on the magnitude and rate of development, hyponatremia may or may not cause symptoms. In general, slowly progressive hyponatremia is associated with fewer symptoms than is a rapid drop of serum sodium to the same value. Signs and symptoms of acute hyponatremia do not precisely correlate with the severity or the acuity of the hyponatremia. Patients may have symptoms that suggest increased secretion of ADH, such as chronic pain, symptoms from central nervous system or pulmonary tumors or head injury, or drug use. Sources of excessive fluid intake should be evaluated.. The chronicity of the condition should be considered. 62. After the identification of hyponatremia, the approach to the patient depends on the clinically assessed volume status. Prominent physical findings may be seen only in severe or rapid-onset hyponatremia and can include the ff. Confusion, disorientation, delirium Generalized muscle weakness, myoclonus, tremor, asterixis, hyporeflexia, ataxia, dysarthria, Cheyne-strokes respiration, pathologic reflex Generalized seizure,coma 62 63. Complications Cerebral edema Noncardiogenic pulmonary edema Central pontine myelinolysis 63 64. Diagnosis SIADH is best defined by the classic Bartter-Schwartz criteria, which can be summarized as follows Hyponatremia with corresponding hypo-osmolality Continued renal excretion of sodium Urine less than maximally dilute Absence of clinical evidence of volume depletion Absence of other causes of hypo natremia Correction of hyponatremia by fluid restriction 64 65. Laboratory Test Serum sodium, potassium, chloride and bicarbonate Plasma osmolality Serum creatinine BUN Blood glucose Urine osmolality Serum uric acid Serum cortisol Thyroid-stimulating hormone 65 66. Imaging Studies Chest radiography Computed tomography MRI 66 67. Medications Vasopressin-related Conivaptan Tolvaptan Diuretics, loop Furosemide Diuretics, osmotic agents Urea Mannitol Tetracyclines Demeclocycline 67 68. 68 69. Refers to the constellation of metabolic disturbances that may be seen after initiation of cancer treatment. Typically associated with acute leukemias and high-grade non-hodgkin lymhomas. 69 70. Pathophysiology Rapid tumor cell turnover results in release of intracelllular contents into the circulation. This release can inundate renal elimination and cellular buffering mechanisms, leading to numerous metabolic derangments. Hyperkalemia is often the earliest laboratory manifestation. Hyperkalemia and hyperphosphatemia result directly from rapid cell lysis. 70 71. Hypocalcemia is a consequence of acute hyperphosphatemia with subsequent precipitation of calcium phosphate in soft tissues. 71 72. Physical Examination Severe hypocalcemia can lead to the ff: Paresthesia and tetany with + Chvostek and Trousseau sign Anxiety Carpal and pedal spasm Bronchospasm Seizures Cardiac arrest 72 73. Deposition of calcium phosphate in various tissue may be responsible for the ff: Pruritus Gangrenous Changes of the skin Iritis Arthritis 73 74. Uremia can produce the ff: Fatigue Weakness Malaise Nausea Vomiting Anorexia Metallic taste Hiccups Neuromuscular irritability Difficulty concentrating Pruritus Restless legs Ecchymoses 74 75. Approaches Urine pH and output Imaging studies Cardiac monitoring Histologic findings Blood chemistry Surgical care Diet Hydration 75 76. Medications Uricosuric Agents Allopurinol, Rasburicase Electrolytes Dextrose Loop diuretic Alkalinizing Agents Antidotes 76 77. 77 78. Any radiological indention of the thecal sac Tip of the spinal cord lies at the L1 vertebral level. Lumbosacral nerve roots form the cauda equina. 78 79. Causes Metastaic tumor from any primary site Tumor with predllection to metastasize to spinal column Vertebral metastases are more common than ESCC 79 80. Clinical Features Early recognition leads to better outcomes Efficacy of treatment depends most on patients neurological function at presentation Median time from symptoms to diagnosis is around 2 months More than half of the patients who present to the hospital are non-ambulatory 80 81. Red Flags Pain First symptoms Precedes other neurologic symptoms by 7- wks Severe local back pain Aggravated by recumbency May become redicular 81 82. Motor Weakness: 60-85% Patients may be hyperreflexic below the lesion and have extensor plantar Weakness tends to be symmetrical Progressive weakness is followed by lost of gait function then paralysis The severity of weakness is greatest with thoracic metastases 82 83. Sensory Less common than motor findings Still present in majority of cases Ascending numbness and parasthesias Bladder and Bowel Function Loss is late finding Autonomic neuropathy presents ussually as urinary retention 83 84. Imaging Radiolography MRI CT sanning Bone scan 84 85. Treatment Pain mangement Corticosteroids Opiates Anticoagulant Prevent constipation Surgery Chemotherapy Bisphosphonates 85 86. Examination Fluctuating level of consciousness Vitals normal, no fever Dehydration Coarse upper airway sounds No other pertinent findings 86 87. Investigate CBC normal Mildly elevated BUN and Cr Normal LFTs Standard electrolytes normal 87