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Internal medicine - questions for state examination Dept. of Internal medicine 1, applicable since 2016/17 Selected emergencies in internal medicine Shock and hypotension Dyspnoea and cyanosis Syncope Disorders of conscious level Metabolic comas Cardiac arrest and cardiopulmonary resuscitation ‘Sepsis, septic shock ~ clinical signs and principles of therapy General aproach to patient with a suspected poisoning Cardiology, angiology, atherosclerosis and hypertension 9." Acute heart failure 10, Chronic heart failure LL. Treatment of chronic heart failure 12. Pharmacotherapy in cardiovascular disease 13, Differential diagnosis of chest pain 14. Acute coronary syndrome definition, sub-types and diagnosis 15. Treatment of acute coronary syndrome 16, Complications of acute coronary syndrome 17, Chronic coronary heart disease ~ ethiology, classification, clinical manifestation 18. Treatment of chronic coronary heart disease 19, Pulmonary embolism 20. Pulmonary hypertension and chronic cor pulmonale 21, Cerebrovascular accidents 22. Investigations in cardiology 23. Aortic valve disease 24, Mitral valve disease 25. Congenital heart diseases 26. Differential diagnosis of arterial hypertension 27, Arterial hypertension — definition, diagnosis, examination 28. Complications of arterial hypertension 29. Causes of secondary hypertension 30. Treatment of arterial hypertension 31. Diferential diagnosis of edema 32. Atherosclerosis. Pathophysiology and risk factors 33. Atrial fibrillation and atrial flutter 34. Supraventricular arthytmias 35. Ventricular arrythmias 36, Bradycardias 37. Treatment of arrhytmias 38. Temporary and permanent pacemakers, cardiac resinchronisation therapy, electric cardioversion, implantable cardiac defibrillators 39. Diseases of pericardium 40. Myocarditis and cardiomyopathies 41. Infective endocarditis 42. Deep vein thrombosis 43, Chronic lower limb arterial disease 44, Acute arterial occlusions 45, Varicies, chronic peripheral venous insufficiency, phlebitis. Nephrology 46. 47. 48. 49. 50, SL 52, 53, 54. 35 56. 37. 38. 59, 60, 61 62. Investigation in renal and urinary tract disease Urinary tract infection ‘Tubulo-interstial diseases Urinary caluli Polycystic kidneys and other inherited nephropathies Renal insufficiency and renal failure. Classification, causes, symptoms Differential diagnosis of oliguria and anuria ‘Acute post-infection glomerulonephritis and rapidly progressive glomerulonephritis Chronic glomerulopathies Dialytic treatment Organ transplantatios Differential diagnosis of pathological findings in urine Acute kidney failure Chronic kidney failure Nophrotic syndrome Conservative non-dialytic treatment of chronic kidney failure ‘Tumors of the kidney Gastroenterology, hepathology 63 64, 65 66, 67. 68. 69, 10. 1 2. B. 14, 15. 16. 77. 2. 79. 80, 81 82, 83, 84, Diseases of the esophagus Ulcers of the stomach and duodenum Inflammatory diseases and tumors of the stomach Chronic inflammatory bowel diseases Gastrointestinal bleeding Malabsorption syndrome Coeliac disease Panereatitis Investigations of hepatobiliary disease Hepatitis and hepatopathies Acute liver failure Inherited liver diseases Hepatic cirrhosis, complications of cirthosis ‘Tumors of the liver and subhepatic space Cholestasis. Hereditary hyperbilirubinemia Gallstones, clinical features and complications Colorectal cancer Differential diagnosis of abdominal pain Differential diagnosis of jaundice Differential diagnosis of hepatomegaly Differential diagnosis of diarrhea Differential diagnosis of ascites Rheumatology, osteology 85, 86, 87. 88, 89, 90. ol 92. 93 94, 95 Differential diagnosis of arthralgia Rheumatoid arthritis Systemic Inpus erythematosus and other connective tissue diseases Systemic vasculitis Seronegative spondarthritis, Crystal-associated disease Differential diagnosis of elevated sedimentation rate Differential diagnosis of fever ‘Treatment with corticosteroids and nonsteroidal anti-inflammatory drugs Osteoarthrosis Osteoporosis, osteomalacia, other metabolic diseases of bone Hematology 96. Iron deficieny anemia 97. Megaloblastie anemia 98. Hemolytic anemia 99, Aplastic anemia 100. 101 102. 103. 104, 105. 106. 107. 108. 109. 110. ul 112. 13, 14, 1s 116. Differential diagnosis and treatment of anemias Myeloproliferative disorders. Myclodysplatic syndrome. Acute leukemias Chronic myeloid leukemia Multiple myeloma, macrogtobutinemia, systemic amyloidosis, Principles of chemotherapy, bone marrow transplantation, Treatment of hematological malignancies Hematological disorders predisposing to thromboembolism Differential diagnosis of bleeding disorders Congenital and aquired bleeding disorders Thrombocytopenia, platelet functional disorders, wessel wall abnormalities Polycythemia vera and secondary polycythemia Differential diagnosis of lymph node enlargement Chronic lymphocytic leukaemia Lymphomas Differential diagnosis of splenomegaly Blood products and saft transfusion procedures, adverse effects and complications of transfusion 117. Diabetology, endocrinology, disorders of metab 118, 119. 120. 121 122, 123 124. 125. 126. 127. 128, 129, 130. 131 132, 133, 134. 135 136, 137, 138, 139, 140, 41 142, Principles of antithrombotic and anticoagulant therapy m and nutrition Hypo- and hyperparathyroidism Discases of anterior pituitary Diseases of posterior pituitary and hypothalamus Hypothyroidism Thyrotoxicosis Goitre, Thyroiditis and thyroid neoplasia Adrenocortical hyperfunction Adrenocortical insufficiency Phacochromocytoma and dif, dg. enlarged adrenal glands Diabetes mellitus (types, ethiology, clinical features, diagnosis) Diabetic emergencies Treatment of diabetes mellitus Acute complications of diabetes mellitus Chronic complicatioms of diabetes mellitus and their prevention Metabolic syndrome Dyslipidemias and their treatment Obesity Malnutrition, principles of enteral and parenteral nutrition Disorders of water and mineral homeostasis Hyperkalemia, hypokalemia Hypercalcemia, hypocalcemia Disorders of acid-base balance Principles of antibiotic therapy Drug intoxication, carbon monoxide intoxication Alcohol intoxication (cthyl- and metylalcohol, ethylenglycol) Pulmonology and phthisiology {AP Respiratory failure, oxygen therapy, ventilatory support aa Respiratory emergencies — diagnostics and treatment Hemoptysis — differential diagnosis and treatment Community acquired infections of lower airways, community acquired pneumonias ¥%I_ Nosocomial pneumonias, pneumonias in immunocompromised host, lung abscess 269 Asthma, differential diagnosis and therapy {Chronic obstruction pulmonary disease and its phenotypes & Management of obstructive pulmonary diseases f Pleural effusion, empyema, hemothorax, chylothorax Pneumothorax, classification, diagnostics, therapy Gill Thoracentesis, pleural fluid analyses Az Lung cancer, classification, diagnostics, differential diagnosis 5 Lung cancer - therapeutic modalities Vl Bronchiectasis, cystic fibrosis, diagnostics and therapy (15. Disorders of the mediastinum ~ neoplasms, mediastinitis, mediastinal syndromes v6] Classification of diffuse parenchymal pulmonary diseases, differential diagnostics Sarcoidosis — staging, diagnostic procedures and therapy Extrinsic allergic alveolitis, drug-induced pulmonary disorders \/ 19, Sleep — disordered breathing, sleep apnea, diagnosis, treatment /20 Tuberculosis — etiology, pathogenesis, latent tuberculosis infection (29 Miliary tuberculosis, extrapulmonary tuberculosis 22. Pulmonary tuberculosis — diagnostics, treatment J23. Pulmonary tuberculosis ~ epidemiology, prevention, pr 2M Nontuberculous mycobacterial infections 25) Pulmonary function testing ~ ventilation, respiration, bronchoconstrictive and bronchodilation tests rronchoscopy, chest ultrasonography, and other pneumologic investigative methods ary tuberculosis ary and postps an adacughe us gent Shock = acute circulatory failure with inadequate or-inappropriataly distributed tissue perfusion, potentially resulting in fend organ injury © Characterized by: hypotension + poor perfusion + tachycardia + porlochuencas Note: ‘Shock’ isnot synonymous with hypotension, which is often a late manifestation © (PRYSIBIOEIESI|(.c. patient’s physiological BP) [B]=Aeate > asocited wishock | + © obstructive: tension pneumothorax, cardiac tamponade, pulmonary embolism + © Cardlogenic: arthythmias, ischemia, valvulopathy, myopathy #9 Hypovolemic +; Dehydration: persistent vomiting, dlarthea,diaphoresi, burn » Senor CI orvereateg: ares, cc, bete-bocker, clonidine, dgxn, sedatives, valproate, TCA CO intonicaton Ell: _sustaotg tyecadreralsm, pafhypertyroidim E+ Post panda FL _Nevrty mesioed hypotension (eg rolongued standing) = Wui0" OE Sy + Severe kidney disease Yj because arterial pressure. Js. determined. by l€aiiae BUEpll) venous-pressure and Syste Vascular tesistane, 2 reduction in elther one orate variables can lead to hypotension © Maintenance of normal BP: ‘ > x v8 + Heartacingasa pune Co | wae + vasculartone 24 D5 gu ME + Volume of erculatng blood (MAP) | + MAP= COXTPR= (sR) TPR-70-110NmB) 9 Or MAP =P + 1/3(SP-0P) - ~ ‘+ Minimal MAP required for organ function: JO mmiig Z | [Sceincua sa sri | eat ee Pagina Lde7 © Cardinal symptoms: ihitheadedness| dziness| ‘© sufficiently iow: fating/syncope | © Other ee + (Syndromes) © |Outhostatchypotensioy = postural hypotension > low BP with changes in poston from seated/lving to standing Up. Tarsent low BF and usualy reresets ein the ronal compensatory ait of thes) ea © Newracardiogeni¢=vasovagal mediated - occurs due to vagal stimulation in frolongued upright postion vc) st © [Post:orandial: drastic decline in BP occurring 30-75 minutes after eating substantial meals (great deal of blood is [/") diverted to the intestines) cis Vo gata cplanchuie. vessel obi € fen woe Adress the cause -Asumatomatic physiological > doesnt require treatment © infidkases \ + Diet drinking plenty offuids, moming caffeine * _Afpre:syncope: supine position with leg iting © nlleveré cases: pharmacological rationale "+ Increase CO: by increasing blood volume & stimulating contractility [+ Pragonists (dopamine, dobutamine) 1290!" 0 *# _xt-agonists« systemic vasoconstrictis (phenylephrine) Increase SVR by causing vasoconstriction ‘ + Vasopressin analogue (terlipressin)/ © p+ vsp! * Sensitize adrenoreceptors to catecholamines: glucocorticods (Fudrocortisone) 3: acute circulatory failure with inadequate or inappropriately distributed tissue perfusion, potentially resulting in lend organ injury © classifi (© Hypovolemic = loss of circulatory volume + Hemorrhagic, dehydration, vomiting, diarrhea, interstitial fluid redistribution (© Cardiogenic= failure of heart to function as an effective pump ‘+ Myopathic (myocardial ischemia + infarction}, mechanical, arrhythmic, pharmacologic (© Obstructive = extra-cardiae mechanical flow obstruction ‘Massive PE, pericarcial tamponade, constrictive pericarditis, increased intrathoracic pressure (eg tension pneumathorax) (© Distibutive = abnormalities ofthe peripheral circulation = anaphlatic= severe allergic reaction Septic whole body response to severe infection + Neurogenic = trauma to SC + Metabolic (e.g. Adtson’s, myxedere, coma) + psychogenic «Pathophysiology (© Nomatter the cause, they alllead to decreased circulating volume © Stages * Anita: J perfusion > hypoxia > + lactate -> metabolic acidosis Pigina 2de7 tivation of reflex compensatory mechanisms: ‘+ Sympatho-adrenal response (RA) ‘+ Neuroendocrine rasonse (release of ACTH, vasopressin, cortisol, glucagon) 1+ Release of pro: id ant-inflammatory mediators (in severe infection): complement, platelet activating factor, arachidonic acid. products, lysosomal enzymes, endothelium-derived vasoactive mediators, ete + Activation ofthe coagulation system + Hyperventiation + a: rogressive: occurs when compensatory mechanisms fail-> tissue hypoperfusion + hypoxia -> MODS {cnult-organ dysfunction syndrome) ‘+ MODS: syndrome where there is a progressive and potentially reversible physiological dysfunction of 2 or more organs + Fist organs to be affected: heart, lungs 1 trreversibie: widespread tissue necrosis > MOF (multi-organ failure) -> death Early: tachypnea, tachycardia, narrow pulse pressure, reduced capillary refi, cool extremities and reduced central venous pressure (CV) ate: hypotension and altered mental status, reduced urine output Clinical examination General assessment + Skin colour: pallor, cyanosis, + Mechanism of injury visible hemorthage * Breathing, hyperventilation + Gitculation: HR, pulse, 8, peripheral temperature + Consciousness: decreased = Urine output: oligoanuria ‘Monitoring + Non-invasive: BP, pulse, HR, urine output = rvasive: MAP, CVP * Doppler: CO, myocardial function Imaging: OF, AXR, ECG Labs: FBC, ABB, lactate, electrolytes, glycemia, uree Cr, cardiac enzymes, hemocoagulation ‘Management: Shock ina trauma patient Is hemorrhagic until proven otherwise Goal: to retuen critical organ perfusion to normal (e.g. normalize BP) 1 Positioning: supine, leg elevation if no trauma 2.Oxvgen therapy 2.Causal weatment * circulatory fallure > vasopressos,inotropes + Fractures > splinting = Hemorshage -> stop it + Tension pneumothorax > neddle decompression + PE thrombolties + ant-coagulants + Tamponade 9 pericardiocentesis + Sepsis > ATBS + Anaphylactic © Adrenaline ~0.5 mg im, Pagina 307 + Corticosteroids ~blocks some effects of histamine (hydrocortisone 200 me Lv) + Heanti-histaminic agents—to prevent further release of histamine ‘+ Bronchodilators~in case of severe bronchospasm (aminophyline, ephedrine) * Unclear > hypovolemia © 4.Getan IV access + PVC (antecubital, hand dorsum) i beter coz cannulas ae wide and bore + Alternate: interosseous, CVC © S.volume therapy + Fluids warmed at body temperatures * Given according to volume loss + <10%-> not necessary to replace fuids + 10-20% > crystalloids/eolids 30-40% > ¥ fluids +% blood + 40% -> blood transfusions ©. Coagulation management: + Co-administered with volume therapy FFP, cryopreciptate, coagulation inhibitors (antithrombin Il, protein Cor 5) © ZAnalgesio © 8.Thermoreguletion: hypothermia D. HyPovoLemic sHocK Most common type of shock Ethiology: caused by insufficient circulating volume (© Exogenous losses ~ eg, haemorrhage (most common), burns, diarrhea, et © Endogenous losses ~ eg. haemoperitoneum © Losses of: blood (hemorrhage), plasma (burns), water (dehydration) Pathogenesis: (© A poor venous return to the heart will decrease the stroke volume and cardiac output (©The patient will attempt to compensate by tachycardia and increased systemic vascular resistance (SVR) + They become cold peripherally Clinica Features: ‘© Inadequate tissue perfusion: = skin—cold, pale, slate-gray, slow capilry rfl, ‘Lammy’ * Kidneys oliguria, anuria * Brain = drowsiness, confusion and irritability © Haemodynamic changes + Low CVP and pulmonary artery occlusion pressure + towco * Increased systemic vascular resistance © Ince tic tone + Tachycardia, narrowed pulse pressure, ‘weak’ or ‘thread’ pulse + Extreme hypovolemia may be associated with bradycardia + Sweating * Blood pressure ~ may be maintained intial, but alter hypotension supervenes © Metabolic acidosis Pégina .de7 © Correlation to fluid loss: ‘class Blood loss Response. ‘Treatment 1 [25 9%(0.751) — |min. fast HR, normal a> rinimal in [5-3096(0.75-1.5 1] fast HR, min. ow BP Intravenous fluids nr |30-40%6(1.5-20) [very fast HR, low BP, confusion |fluids and pecs iv [a0 v2.9 ertical BP and HR aggressive intervention E, CARDIOGENIC SHOCK ‘+ Ethology: caused by the fallure of the heart to pump effectively (MI, Acute Heart Failure) © Other causes include arrhythmias, cardiomyopathy, congestive heart fallure, carclac valve problems ete + Pathogenesis: ©The patient will have a poor cardiac output and will therefore attempt to maintain a blood pressure by increasing sve (© Blood pressure can be low, normal or high (© Organ perfusion is compromised, peripheries are cold and the patient s prone to pulmonary oedema © Clinical Features: ‘© Haemodynamic Changes: Signs of myocardial failure ‘+ Signs of myocardial fallure (eg. ralsed JVP, pulsus alterans, ‘gallop’ rhythm, basal crackles, pulmonary oedema) + Early echocardiography Is important to assess contractility, valve function and exclude significant pericardial effusion + Increased! systemic vascular resistance (SVR) + CyP and PAOP high (except when also hypovolemic) + Mortality —high (90%) ‘+ Requires parallel therapy of shock and the heart F. DISTRIBUTIVE SHOCK + Peripheral vasodilatation and subsequent maldistribution of blood flow leads to a relative hypovolaemia (There is more space in which to put the same volume of fluid) + Common examples: septic, anaphylactic and neurogenic shock G. NEUROGENIC SHOCK + Very rare form of shock + Ethiology: caused by trauma to the spinal cord resulting in the sudden loss of autonomic and motor reflexes below the Injury level ‘+ Without stimulation by sympathetic nervous system, the vessel walls relax uncontrollably leading to a sudden decrease in peripheral vascular resistance, and consequentiy to vasodilation and hypotension © Especially inthe splanchnic region and in the muscles ‘© Features: hypotension, bradycardia, warm peripheries, venous pooling and sometimes priapism gina § do7 Bradycardia results from unopposed vagal activity and has been found to be exacerbated by hypoxia and fendobronchial suction Note: bradycardia is an important feature of this shock; if hypotension and tachycardia are present, e.g. nan RTA Victim, look for other causes of shock lke external or internal haemorrhage HL ANAPHYLATIC SHOCK Causes: a wide variety of allergens (Drugs, Vaccines, Insect bites, Snake venom, ete.) + Glinical Findings: L. Sepric sock Signs of Profound Vasodilation: Warm peripheries + Low 8P + Tachycardia Others: + Erythema, urticaria, angio-oedema, pallor, cyanosis + Bronchospasm, rhinitis + edema of the face, pharynx and larynx + Pulmonary oedema + Hypovolaemia due to capillary leak ‘Nausea, vomiting, abdominal cramps, diarrhoea Haemodynamic Changes: = Lowsve "Low cvP and PAOP. = High co + 95% of cistributive shock + Cause: circulatory fllure due to overwhelming infection + Stages: ° eco 0 Sepsis: symptomatic bacteremia, with or without organ dysfunction Systemic Inflammatory Response Syndrome (SIRS): whole-body inflammatory reaction against microbes which entered the body through an infection Severe Sepsis: sepsis associated with organ dysfunction, hypoperfusion or hypotension Septic Shock: acute circulatory failure characterized by persistent arterial hypotension despite adequate fluid resuscitation, secondary toa documented infection Gram- bacteria: e.g, Escherichia col, Proteus species, Klebsiella pneumoniae, ete Other causes: some gram-positive cocci eg. pneumococci and streptococci, and certain fungi ‘Git (20-40%) Chest/Lungs (35-50%) Uni (10-30%) Soft-tissues (5-10%) + Pathogenesis: Endotoxin-mediated activation of acute phase proteins + complement and coagulation cascades -> hyperdynamic state (‘SCO + SVR) -> marked capillary permeability > third space loss > hypovolemia > hypodynamic state (¥-C0 + SVR) Hyperdynamic Hypodynami increased CO and PR, decreased BP and SVR ~ different clinical signs mii to hypovolemic, often DIC gina 6 407 APPROACH TO SHOCK =|) Pigina 7 de? LYBES OF SHOCK {SHOCK SYNDROMES}: ° > Most common) used by loss of circulatory volume: blood, plasma or water May be an endagenous or exogenous loss: Endogenous: Haemoperitoneum, asctis = Exogenous: # Bleeding (Hemorrhagic shock) > Most common ‘© Burns (loss of plasma} ‘¢ Dehydration e.g by severe vomiting or diarrhea (loss of water)# , mortal — Caused by failure of the heart to work as an effective pump ~ Causes: Ml, Acute Heart fallure/Congestive Heart failure, Arrhythmias, Cardiomyopathy, hypothermia (bradycardia) (3) bistaiaorve — SEPTIC SHOCK > 90% of distributive shocks N - NEUROGENIC SHOCK “6 ssrauCTIVE > Caused by aneattacardiac obstruction to blood tow = causes: > Pulmonary emboli (Thromboembolidsease) > Rott eenoss ® enon peumethorx (intrathoracic Pav to accuriaton of arn Itopleuel space causes Shifting of merlastinum towards the contralateral side casing obstruction of IVC) road pericardial effusion progressively compresses the R heat (due to softer wa) towards Gre Crear (w/ thicker wa eausing a dof blood fow ram RtoL se) While assessing shock, always take in account the primary cause > evaluate the classic Marinum triangle Cardiac output ei a 4H: Hypoxia, Hypovolemia, Hypothermia, Hypo or Hyperkalemia 4T: Tension Pneumothorax, Tamponade, Thromboembolism, Toxicities SVR oe (afterload) (Preload) SHOCK SYNDROMES (Pathophysiologic changes}: Pathopinysiology: = | hin circulatory Volume (poor venous return) > J CO J ap 4) BP > stimulates Baroreceptors > + SNS (and |. Ps) * TSNS > 4 SVR (through vasoconstriction) and T HR: + [EWA ato seen eve to blood circulating nw. (venous return) + ¥.CO+ vasoconstriction leads to hypoxia > Tlactate |<.) “Sin gld ale, mottled appearance (marble ike), (due to sweating by SNS) * Brain: somnolence, confusion, = Kidney: Otigutia or anuria, c - ) (25 a compensation for metabolic acidosis) Correlation of symptoms to fluid toss: © 0-100 (0-500 mil}: No signs of shock © 10-20% {500-1200 ml): Mild shock —poor perfusion of the non vital organs (skin, muscle, fat, bone) + Coo! & moist skin, Pallor, fachycardia, 8 normat and concentrated urine » 20-4098 (1200-1800 mi}: Moderate shock ~ Coot & moist skin, Palflor, Tachycardia, weak plfse, BP 100-8omméte, oliguria, confusion/agitation >40% (>1800 ml}: Severe shock ~ 8° CO > x) blood Row to tissues > BP * BP > stimulates Baroreceptors > “P SNS {and WPS) * TSNS> 4 SVR and ‘P HR only if heart is able to respond, otherwise bradycardia develops + There is anf Cve|due to blood pooling in w. fo eo * L blood flow to tissue > hypoxia > 4 lactate fo stupor and coma Giinical findings: * Skin: go! and gyanotie(due to blood stasis and consequent accumulation of deoxy) Brain: somnolence, confusion, ivitabiity/agitation * Kidney: Ofiguria or anuria = Bulsus alternian (alternating weak-strong pulses) cok cho celts + Tachycardio/Bradyearda, yp fou + Hypotension (HYBEREAEIBHA 2s a compensation for metabolic acidosis} 5) bisraiaurive soe “Pathophysiology: «Possible cause leads to s) SVR > peripheral vasodilation and maldistribution of blood flow (blood stasis) > | BP + ¥BP-> stimulates Baroreceptors > SNS (and J Ps) p lurcnoule watony a'slumloance «SNS > no effective 4 in SVR Gui to persistent peripheral vasoditation but there is 7 HR + ace. to equation: LMAP + There is a CV [bes blood poois in periphery and there is, venous return 1g leads to hypoxia > 4 lactate W's a severe form of sepsis (systemic inflammatory response to infection) in which there is an acute circulatory disturbance and consequent tissue hypoperfusion w/ signs of shock The circulatory disturbance is caused by the invasion of pathogens (most commonly G- bacteria) which tigger an inflammatory reaction w/ release of many inflammatory mediators (e.g vasoactive susbstances {histamine, serotonin and bradykinins] promoting peripheral vasodilation > better access of the immune cells and mediators to the pathogens tbe in tissues Ctinicat setae © Body temperature € 36% oF> 38°C) Tachycaraia> 90 Bont <4slefe o lation - respiratory rate > 20 breaths/min( oP blood pCO2 < 32mmHg {hypocapnea) ° fuosand oa Skin, atm due ta vasodilation} * Brain: somnolence, confusion, irritability/agitation. = Kidney: Oliguria or anuria + Bounding uls¢(srongpuse) 09 ~ st -OF = Tachycardia bd ANAPHYLATI It’s @ severe form of anaphylaxis (ig mediated allergic reaction) in which there is an exaggerated immune response to an allergen triggering the release of high numbers of chemical mediators by degranulation of mast cells and basophils, ‘causing massive peripheral vasodilation Glnical findings ~ [SignsioF anapiylaws (ABE atFection) Cutaneous manifestations: Urticaria, erythema Quinke’s edemas > edema of face, neck, larynx and angioedema Laryngospasm, Bronchospasm, Dyspnea GIT symptoms: nausea and vomiting Circulatory disturbances ‘ombined w/ Bignslohtissuelhypopertision: care Bhi to vsedhion = Brain: somnolence, confusion, irritability/agitation = Kidney: Oliguria or anutia "Tachycardia = Hypotension C. NEUROGENIC SHOCK (very rare) i's a trauma to the spinal cord leading to sudden loss of motor and autonomic reflexes below the level of injury (UMN lesion) SNS J SVR ~ Peripheral vasodilation (specially in splanchnic region and mm.) Clinical findings: = Signs of SC lesion: (© Spastic paralysis and “reflexes ~ Combined w/ signs of tissue hypoperfusion = Skin: warm (due to vasodilation} + Brain: somnolence, confusion, iritability/agitation © Kidney: Ofiguria or anuria = Hemodynamic signs: Bradycardia due to unopposed vagal activity = Hypotension 4 OBSTRUCTIVE SHOCK Pathophysiology. . he PCO due to J amout of blood coming to the L chamber > J BP | BP > stimulates Baroreceptors > 1 SNS (and J PS) =P SNS > D SVR and THR + Theres anf Cv} de to bleed potng nw. * J blood flow to tissue > hypoxia > 4 lactate -» Moc Clinical fincing ° ‘Snot musa > edema of the logs, face. skint Sees BBN f'7 cosine loupouas : dette. ahaa bie aeea tee + Tachycardia 40 Wully Jutivg inepiadio ~ [EYBERVEAIANI fas a compensation for metabolic acidosis) itability/agitation Regardless the cause of shock, itis always characterized by tissue hypoperfusion being a progressive disorder that f not treated leads to death ® cotta, en Hvpopersion mitochon dysfunction > anaerobie metabolism > Lactic a, Accumulation ‘> Metabolic acidosis — eo emperor non-nareg Body activates mechanisms that Baroreceptor refiex > ERISNS! in order to maintain 8% and CO > vasoconstriction (P SVR and 7. HR + silmullo.adrenal.g.to.release Epi and NE for further = Hypoperfusion of kidneys > activates RAA system > + fluid retention and Vasoconstriction in order to “P BP (Oliguria or anuria) 4 ADI sectio- ‘Hyperventilation.as a compensation of metabolic acidosis (in v9 ap lors Pe G ry > MODSievelops. ~~ When compensatory mechanisms begin t(a.bnd vital organs start tobe affected ©. Severe hypotension, confusion is evident, hypoventilation, bradychardia may develop = There is worsening of the condition w/ severe metabolic acidosis, capillary damage and ‘P capilary permeability > further fluid loss into interstitial spaces > edema @ Refractory/tereversible >|MOEdevelops, MODS = Multiple organ dysfunction syndrome > Jarcrowal cayen (arg & ‘When 2 or more organs begin to become dysfunction and failing irreversible damage to organs with definitve failure vouges Chg ARDS « Mol ORGAN DYSFUNTION © Luss > usually the Hobe atfected! ‘Shock lung devetops (ARDS) due to diffuse alveolar damage = & perfusion of alveoli > ventilation:perfusion mismatch > disturbance of gas exchange > hypoxemia > damage to alveolar capiltary membrane > ‘F capillary permeability > interstitial Jung edema + damage to surfactant w/ development of Microatelectasis > Att ARO) (1 (a0) , pat, ) Gokoners > tobe affected’ Kidney hypoperfusion -> damage to interstitial and tubular nephrons > EAT > oteuria or anuria > inhability to concentrate urine -> accumulation of toxic metabolites in circulation (@HAEMGCOAGULATION DISORDERS, = Due to damage to vessels and capillaries there i activation of clotting cascade [> great depletion of clotting factors w/ bleeding diathesis and formation of multiple intravascular microthrombi DIC), @ Hatt = Hypoperfusion of coronary aa. -> Myocardial ischemia >/f4l pnd subendocardial haemorrhage @st ~' Hypoperfusion of splanchnic vessels > ischemia to GIT mucosa (schemic colts) » haemorrhage > damage of ucosaallows the bacterial to gain access to circulation. @ ser, ~ Hypoperfusion > Fatty changes and hepatic dysfunction w/ inhabilty to eliminate toxic substances or pathogens > lungs and other organs are exposed to bacterial toxins and other inflammatory mediators @as ~ (RRRRRRRERRIcEpNatopARycharacterized by confusion which progresses into. stupor and coma ‘Always look for signs of erculatory disturhianic® and hypoperfusion of organs (bcs it means organ dysfunction) ‘HESWBAVlot pt nay help in DX General clinica! signs: = Signs of confusion, agitation or irritability (brain dysfunction) = Skin changes: * Cold (Hypovolemic, cardiogenic and obstru: Pale vs cyanotic = Mottled appearance (marble Hike) = Moist (due to sweating) ~ Circulatory changes: = Hypotension = Tachycardia (or bradycardia either in cardiogenic, neurogenic shocH or in advanced stages of shock) Pulse: weak vs strong, pulsus alternans, pulsus paradoxicus = Pulse oxymetry: 4} Spo2 = torte = Capillary refil (*, except in distributive) = Purine output = Changes in repiratory rate, initially Hyperventilation but in later stages hypoventilation "Laboratory tests! ~ Blood gases pt, J-p02, C02, # lactate, JHCOs , Nat, Ch, K+) = CRC (RACs, Hb, HTC, Was, Platelets) + S-Electrolytes, Sgiucose, S-BNU- - Haemoeoagulation tests ~ Urinesanatysis: % ~ Acc to suspicion * Cardiac enzymes > Troponin tor T+ myoglobin -> cardiogenic shock * CRP or Pro-calcitonin > sepsic shock ) vs warm (Distributive) Echo Doppler US > cardiogenic insufficient heart pump and SV) or obstructive (® sided dilation or compression) - = Ghemray> Tension Pneumotherax = Inyesive procedures (MAP and CVP measurements) are usualy not performed due to instability of pt VARIANTS HYPOVOLEMIC | CARDIOGENIC | OBSTRUCTIVE [DISTRIBUTIVE co + + + * HR + ‘a * ‘md SVR + + v + BP v + v ¥ uve + t t v remenue| s ‘ . in neurogenic shock not 4 in HR but L —_— a Mea)eoncenn? not possble,treat the most likely cause.-> hypovolemic or septic shock reg dike Always provide!®2, ventilation and girculatory support Ie soda Most of the times sedation is required due to confusion, agitation, etc. > helps to | 02 demands q 7 ‘econdingto thcalsey @ ftypovolemic shock > ivfluids) Goal: restore circulatory volume to improve CO and BP and thus restore tissue perfusion Types of fluids which can be given © Crystallold soltions + €uloncod co, ( #904 actole, Hosviolyies © Colloid solution (Volume substitutes or Volume expanders) © Blood products and derivates (Blood transfusion) 1 Blood transfusion air: 1 FFP to packed RBC ee . Therapy <10% 7 No therapy 10-20% Volume therapy {crystalioid/colloid) 20-30% Volume therapy and relative ineation of Blood wansfusion 30-40% | 50h Tals and 50% ood vansfusion OR fllndcation for biood wansuvon 0% Absolute nication of blood tasfsion - Positioning may help {legs are raised as a 1" aid) ‘Volume overioa sided kof ung ede) Aadacnaly some notO0@s may improve the ps state Out nic shocic : aes uf) ~ tn hypothermia > warm the pt, ECMO (Extracorporeal membrane oxygenation) may be required ise Vasopressors (vasoconstrictors) ‘A. Septic shock B. Anaphylactic shock: STEMI Gs gm aduls,03 mgm chen ~ ivFluids = Aekitonaty: "03, Carteasterids) hydrocortisone 200. mg), ARKEHA! (cetiriine), BFSneheAllator {salbutamol) _Nerogenic shock = iv fluids = Atropine (due to bradycardia © onsmaive sno, ~ Tetsion Eneimathoca > TRRRERRIEREEAE for Prete ~ Tamponade > Pericardiocentesis (aspiration of blood) “Pulmonary embolism ->"thromBoyties(Atepase) Remember that peripheral venous access is more useful than central one bes it’s easier, faster and safer Gold extreaies boo =—, Cae ws Reb SB Ryd ve WEISS, we ous are oe oS Ele fo ne vwohees TE Newgate 2 peer ut ~ deren, biz Ly chalieF Fivemeus poo og: 7 @ Sus odie be i bens Lek = ete rperies Ks Webi) putt cena, meso dt - tHe, re > (vast) , 7 Wek ons shbe Areoeren Bypessne Elecbwly ks Qpes 24, 5- 32X10" we Dolo, — (ar dvac tby cs A — Hae —vceag Cenere itary aga ‘© Definition: inte according to his or her level of fitness and exertional threshol for breathlessness © Dyspnea a subjective symptom ands cononly row a shores of reath ott 2 [ier sings) ° ‘Kansieonedtnin-ns)] + Gilt causes acs « (GERERIRESHUREREI «, acute Mi) + CliFexacerbation'/Lv failure] f < ummmmmmormmmmmamny J {Coy stops > deepuan om \ytve, down + Cardiac tamponade a + Upper airway obstruction (anaphylavs, foreign body, mucus plugging) + iway disease (hina COPD etacebation®, rons) + Parenchymal ling clisease (ARDS, phetmonia) + Pulmonary vascular disease (BE vascultis)> Good paslease's Sie + Pleural disease (prieumothorax, tension pneumothorax) + esptatory contol metabo seo, AA, oly) ‘* Valvular heart disease (e.g. Aortic stenosis/mitral stenosis) © Decreased CO. SH crested na papeaae + aves + Pareryma anges erst dase) Pulmonary vascular dsease (pulmonary HTM, vscutis) + Please (effusion) © Gas exchange (infection, emphysema, fibrosis, etc.) © Airway cisease—asthma, COPD, “Hematologé causes: Severe anemia + Cine niuey, ‘+ Polymyosttis, myasthenia gravis, Guillain-Barré syndrome = Kyphosotoney + Othe + Deconahioning (feycatahate coudthow) © IBGRy/keafisocares symptoms anc signe key tothe anpropriat diagnos + Perstent VS intermittent on exertion) + Acute VSehronie Page rot + [Bosition! orthopnea (breathlessness on lying flat; common in hf}, paroxysmal nocturnal dyspnoea [ovhen a pati + Mejorjriggeroccupational, allerges = Chevne-stokes respiration: severe heart fallure woken from sleep fighting for breath Ataf 9 5 gnc: certs poe syaane aanke aptofo ih q ain With cardiac ischemia Avagl 4 = Fever, cough and sputum with respiratory infections = _Unticaria with anaphylexis, wo wociels) = Wheezing with acute bronchospasm Aste ofheaw breathing ypc of decondtoning// © $BC+fferentia (hematocrit to exclude anemia), electrolytes, consider ABG © CAR (hyperinflation and bullous disease suggestive of obstructive lung disease, or changes in interstitial markings consistent wit inflammation, infection or interstitial fui) © Canolac enzymes and ECG If considering cardiac source © CL chest usually isnot indicated in the initial evaluation of patients with dyspnea, but can be valuable in patients with interstitial lung disease, occult emphysema, or chronic thromboembolic disease (PE) © ABC'S: send to Emergency Department in severe respiratory distress * NOTE: Contraindication to 100% oxygen: CO2 retainers (e.g. COPD) ‘= © Cause (central): deoxygenated Hemoglobin > 5 g/dl (i.e the 0, saturation is < 85%) or (© Methemoglobin>1.5 g/dl or Sulthemogiobin >0.5 g/dl ‘= Cause (peripheral): peripheral vasoconstriction and stasis of blood in the extremities + Precautions ‘© Gyanosis appears when a least g/dl of Hb is deoxygenated (desaturated) <¢Gesmzmir teen et ray no appear cyanide hypoxia Polyeythemic patients) (e.g. Hemoglobin >17-20 g/dl) such as those with COPD, Pulmonary Hypertension may appear cyanotic i mild hypoxia ‘© Dermatologic conditions may result in blue skin colour that mimics cyanosis in the absence of increased levels of @ceuss droge tin py es +> canal ranosil th = cWsintracranial hemorthage, cerebral anowa, drug overdose (ex: heroin) + [Respiratory System bronchioii, bronchospasm lng disease, pulmonary embolism, hypoventilation, co ‘duel iho © Pee Boat iffaan Sates “s_ {cardiovascular System] congeitatheartikease, heart fale, heart vale disease, bl Va! (o pla. STEVES) 65% : polycythemia + Serum plucose: to detect hypoglycemia * Infections: LP, urinary culture ‘+ Arterial Blood Gases (ABGS!: cok Arterial PO: to confirm central cyanosis : S02 not a8 good aw indicator due to Increase fetal Hb affinity for 02 (left-shitt) ‘© Increase PaCO2: may indicate pulmonary or CNS disorders, heart failure © Decrease pH: sepsis, circulatory shock, severe hypoxemia ‘* Methemoglobinemia: Decrease $202, normal Pa02, chocolate-brown blood ac) ®@> tamaateme Thee frloaed aaa 1 [Al counonciare gga * Arterial obstruction, * Cold exposure (due to vasoconstriction) + Raynaud's phenomenon (vasoconstriction) ( . »., tS eaard ideas © Management: feat the underlying couse lary refill time wy Pagaaof3 = Teaustent lose of consecournece w/ lore of posianal sion uruatly dio '0 @) SYNCOPE {los Plu Bn ino Balin ratae acne) > As dunaclepized bys) sudden £ douse Eo eletbeatt shott ditaou, sponlauans ecavety € Showtd be aibfenaukioke Your LOE of cten Coster s ko —T—4 howd [re Falls gouseicus ns Thoukat? Rapid Ont? Shenk Dssorin? NOT Sroulannons Renunny? Goma Sudden Hh Conese Anvsst ys¥ ° Frosh -LOC Nonbraiabc — Trassnahe J / poy he Maps in \ Tf no gebal neal hyena kin — shad net be dvaguesed as syncopt: state ic Aisorders + ipforicalion 2 vanlabrobsilan Tih (ARepalluckle — fallurfs bess ef contecousve's) > palyycoguace Proprone oF syncope oak clways corm > wacllvess Aa ness, Geght heacednass OR GRaytag oct of consciousness 9 Gyocope wey be lowed by fohgus, PRESYRCORE = SBS of predRcws® Clout oss af postural fous on LOC 4+ Lay dawn Ma ph Csuptus) case Yn tag m a3eitaka to btesd tous PATHOPUYSIOLOGICAL CLASGI FICATION OF SYNCOPE | © REFLEICDEDRNUYAMENEDRIOCORE — hos; cop tons @Oummmme 3... Skenmmmomepegimtes EN LO ~ vadiabss by Bouchet (foe pin, (nshaanselaben, bled phic ~ mediatyd by cathorta hc shress - Premoushony sgusphoms / prectpitahing fackons 2» grotowau dua to} be calles <= * vogafl © > Cough , Snare ‘ ‘efile stiadaon (sallow, dfecalign, visesnal psi) ee = post -prandal ~ alls Cusaghtlfting lasight.--) (duc 4 Wyporsenstiewity of cotoled staus © 4 oy ~ head Relchery 6@ prssians one conchel Kinas > AIRRORENEORES (1 opparest triygea) 9 AUS, impor v a 7 cLsne, muaihipls systenspbeoply Poelleusen’s de wolasstonowie (oclesne, Lewy boty dena, ~ DI asylordogis, wnasruce spinel cond inpunies ® ® 0 faa @® a 7 yasedlatons, Acurabes pluuctheriras, cub depressacy ~hasnorhage ,diarahae , vowing. ORT oe oigsonc formed = SERRE © es Rese ee ote Finckucl Sic sinas iy.) \- AN con ic as Ciscoe CAN bloc, dees itapleated daceci? mal fianchon dinal ~ Mane | ~Suproventrica «fl, A Pllice’) ~Veakrialor acon | Scoad dest, © SESE sain on bachycandia cee ) ATUL (ecchusce Iagperchnephiey cc MESS, pericardial Aistast /taupoac conta axrousckies of cononany &. ~ Others = PE Jacke aopbe des 28 Ar 0M S45 dos tanietio Low BP/ deal unirro ropension), dus be (Ypemfegronel RAY) odang incaccacl ANS Facury \ st © strachunal Aswaugeey AWS A © wsodspnessens — innova omadaquake veces neuen oH ? cardwac anahytinig “ * comasae Haclowat sinus | se * cosediowrlubibonsy —innuprep Rah CORAOGease MLE wells in OR bGox Syncope LS snfarithet inappnoprcats Respoate bo sceae frigg SHER —svasodilehon asd for ba VBP cu global Gosbnot bpenfenen joebenn © Onlbedabe bypehaanin —sypeo “AT Srapadhene VRP 2 Candiae syncope ealhinigg eoe—a liad bo haascdynamie. compacamaut aS Secnabieel bee x oPkaacspasibion bo syncope = WP sy) = Brugada ay ~ Prcleugeed QT interval Steuchusal —s vshun ciaaiedony decease cabicacqyt He vaspateed abitilyeg Ihe baci bo bis caep oath posucdionce of fine foznt ak 40-20 ye RAQGERISTREBE «5 the ESHER <8 feet mest commen! PaRdioNGscakeR Gyno =O is more Your uact im vataycld pts © RK STRATIEICATION, SAN FRANCISCG SYNCOPE RULE rcuess) ~ sqvcteicts sheak rue nest ef siReeReureuaN” aggshve WE hiskany pasnchoensd < 307 eG abwamal fas. cf brat Bh sbolic BP <4 rally ook hraege, @ in,nitsone ofabes me essence of b =D) AepReactt OW piercer ~ fr on : = was Weta { — couspleds. congecouanssy/ ifr [os Toons to] aap cass Gabon dune? = SPCVARKCES RECNORY Whoret eq Meller ~less of grshunal hous fe? elk posh <2) — trigntyalaugsgueceps lec fhe. Vee casues for S25 )duniuy (GReguHEps KyRCeH /pEgaCepE 5S ~ Past mecr cal Nrslory clnigs y comonbiddties —Reslunal BP aud HR ~ Gardécvascaling, , gsspinatory curcl nesclogce axcrnenahor. 9 ECE M12-Leach) © hacdhucle glascose 9 lab inveastvaahen + -CBC eee = alechedksjts ~ BON eR NIK - AAG penn “Ca Rh scRken wg a Soawchor “2am ceernanaeIN Chettew)) © Gronesse we Sad beck ° Gathestabe challa gp { achive Sasutiag. i fle bashing, *Naanological teats [89 ~cT/MRI ~caRohd dogple > Garohd gauss task misuetesl Loach [Ddx| ° E prlepssy * aasra, myclonic/ mycclicure gers , ideahfeble Krugger, altered onecthing, ayeuoss nconbresce, Fugue billing, postidal dRowsniss fewfsien, cassie —Caon't feagel abo abseat fet) # Uy pogigcaias Wuaxor, hace, perspinahen, LOC Jasee ness 2Enthestabic hypolaswon © cn shauckeg thon lyresge eAnvizhy: humeosblabon, aoe, secs, Loc] ght “ owshn Genaral peruciples inas — G, (ese sel” a 5 Refs Syncope] PATH teasing, Physica cocnten = & 9 CROSSING Coadwae PUGUG, Linpls pecatrst play Tope J Aocaesh cndecinhhifory REspoue cams, monitorsss) > Thidodrcus — in vosovagel sync 8 Cathestehe hy pebession ws -adaguads Inydaabion f sol inle ke wapitodais Logg began eta + Waclrecorhscae J} aiftacchve fheenpy * Pen + Medoustucl binders / sepponbuc Stocktiags to V veucus pecking pits crt Wanoessias (PCI * Condtac crehgthusies y = Sinus nods dgsfasschen oRdiar pacusokee taliuacucle dios thet srcacenah bea dycandke ~ AY conduchon AKER —____ cardiac pacenaker ~ Rererysmal SVT oad VE — oPAVART AVL, aleced Father, — catluhirabletion OAR ——radecoutvel , ahythr coulnel © Torseckes des Reakes —— drscowhnas class ie giug QTeahervel THE dear therapy cancdccurticon ((CD Thenricwt — Reade © BBE clorserat coxssedby syncope apisvecle sh caadieguate —podssth to Gree legy =e hon candogpsce —> cschargy & fellow -BP + Qubizat aducatlor — avoid trgpees — pct ° © Basedou ‘A. perinmion€onsiousnessnenniakaunswifowarenesh self and suroundings, © Consciousness is dificult to measure directly but tis estimated by observing how patients respond to certain stimull © Components of consciousness: RAS B, BACKGROUND: Physiologic Basis for Consciousness © Our state of consciousness is the product of complex interactions between parts ofthe reticular formation, cortex and brainstem, and all sensory stimuli + Reticular Activating System (RAS) © Loose network of neurons and fibres extending from lower brainstem to thalamus © ttreceives input from spinothalamic (sensory) pathways and projects to the entire cerebral cortex ‘© Arousal dependent on the adequate functioning of the RAS ~ thus, Its purely a function ofthe brainstem Signs that the RAS (brainstem) is functioning/intact: patient opens eyes when their name is called (© Modulates incoming information via connections to the RAS + “Therefore, the cortex requires functioning ofthe RAS to function itself co Awareness, means that the cerebeal cortex is working and that the patient can interact with and interpret his environment + ttean be assesses in sevreal way but one tends to focus on(fout areas of cortical functioning ‘orientation, attention span, language, and memory (both hemispheres): generalized severe metabolic or toxic disorders (eg. alcohol, sedatives, bee memspneres ant uraemia, septicaemia) depres overall brain funtion & Lounsge by hypoxia, ischeca, i p ds aera eae mice: Le thenas, — Pacad Onvrous on didset docriogs to Qecrn sleue sg ye bo Rater Slee © Direct effect within the brainstem: a brainstem lesion inhibits the reticular formation, © Pressure effect on the brainstem: a mass lesion within the brain compresses the brainstem, inhibiting the reticular formation + Note: © Asingle focal cerebral hemisphere (or cerebellar) lesion does not produce coma unless it compresses or damages the brainstem ‘© ‘Any condition that increases intracranial pressure (ICP) may decrease cerebral perfusion pressure, resulting in secondary brain ischemia ‘+ secondary brain ischernia may affect the RAS or both cerebral hemispheres, impairing consciousness + £4. cerebral oedema frequently surrounds masses, increasing ther efects ‘+ Prognosis: impaired consciousness may progress to coma and ultimately to brain death WALL TAY QUANT TATUE © Alows meaningful understanding of self and surroundings. s «len aoe ~ plays Cool, fen infecrina. w "Confusion, 1 + Memory cisturbances + Illusions © Hall * beleiowy Page 10f5, setoot + Hotseinations He ‘Caton cous ee) > cxgontawls (4 © Clouded = reduced wakefulness and/or self-awareness, sometimes with confusion © Obtundation: arousable to stimul, decreased alertness, slowed psychomotor response om Somnolenty L © Latha (drowsiness): sleepy, poorattention, fully arousable + Oriented when awake butilett alone willsleep 07 Stupor «sleepy state from which the subjectcan be aroused by vigorous or repeated stimulh 0° Coma = unrousable unresponsiveness systemic causes @ Cerebral hypoxia or hypercapnia: Resplatory falure © etal arsine ares, nypotenson (0 ony cus of shocie) <2) Metabolic disturbance, + Diabetes mellitus " _Myxoedema coma (hypothyroidism) Hoan’ cicoD Ns SOG |. A recta. a ald ce : aT cho 4 BAAS + ADH — aifuhowal hapohtl * Hypothermia |" eee : aly cowie pltecuoue o# ollie siier Mio Jove of wourere af gent Cerebral contusion, Extradural haematoma, Subdural haematoma, (Dinfection: Cerebral abscess, Encephalitis, Meningltis (hnyes,echusin roie'es, ony A Sechiouaae diene Intracerebral. haemorrhage, Brainstem infarction, SAH, Cerebral. venous sinus “heomboss adiohe | oMeetebraltumaut + 4 ICP J wicrad porParton, © Balen Cinsdivg corence no ceieusns, no m- cont acchons) © Hydrocephalus Et ® (DIAGNOSTICAPPROACH 1. fn : ale anseN G Mo Ge cavers <> pulse ovyusr ohontrast CT, as soon asthe patients stabilized 8 4 ‘peaswement of ICP © Sometimes . + diagnosis isunclear: lumbar puncture oF EEG Le CSF rramnalion ly oll cele eho abrous ectoxs ination) 4, 9 ON, ct cidolules, Ugh ut, nd ele Bc + Sep'y toad illeuss 1X of underlying drsotden Hf erdclyag sen rage 2065 dice: Aidvnond_Agilabin Secabiou seals ( RASS, Y Asseres how aptlajed oe sedated vx Mx f + [Glasgow comascaie) > Noewe® Scofes AS © EvBopening (I: Spontaneous &/ To speech3/ To pain2/ No response 1 © Mototresponse (Ml Obeys6 /LocaliesS/ Withdraws 4 / Flexion 3 / Extension 2 /No response 1 © Verbal response (Vi: Orientated 5 / Confused conversation 4 / Inappropriate words 3/Incomprehensible sounds ° ° ° 2/Noresponse 1 2 /25\s% ocoluaciiso’ © nero = sieabinle gles doweyt to pp bat “Hlertness welche © Be “Merbal stimulus stimulation > decors stimulation ih r le timulat (awe ie fe) > Avise Addurle d 3 plnod wl Sixcssorsve dx “ou He chogh Jong: D indaleglrion T "Lower] poss § Gee, deco foul) Corderosw) > Aous odducled @ srleuded ~ | ponaed nag suf glavton Pai i" ecod fiupons, le eats, lags © to 4 ve both coah'c ws ple artendod & mle Faroe ¢ Telsen o. [omaesic VALUATION) © Taking a compl prior events is critical elf bout the time course forthe chanep Jn mental satusapd shout posible causes (ee, recent travel, ingestion of unusual meals, exposure to possible infections, drug or alcohol use possible trauma} © Head trauma; periorbital eechymosis (raccoon eyes), ecchymosis behind the ear (Bate sig), hemotympanu, SF thinorthea and otorrhes © Hypothermia Environmental exposure, near-drowning, sedative overdose, or Wemicke encephalopathy © Hyperthermia; Heatstroke ‘© ewes, etechial or purpuric ash, hypotension, or severe extremity infections (eg gangrene of one or more toe) Sepsis or CNSinfection Nectle marks: Orug overdose (eg, of opis or insulin) ‘bitten tongue: Seizure © Breath oir: Alcohol, other drug intoxication or diabetic ketoacidosis + srolgi xanaio) should focus onthe flowing © @LeveLof consciousness (6C3) ‘o@éve examinations (detailed below) + Puplaryresponses, + pupils + GERBER « poo's, chao fo HNhng? moans, eo-04 siophtalne + ash > popilloedena, ahival baw ouhoye + Other neuro-ophthalmic reflexes ‘o@ Matar function (eg, fscicity, hemiparesis, asters, multifocal myoclonus, decortcate or decerebrate posturing) co(itbaep tendon cefiees (Asymmetry of tendon refexes and plantar responses: both plantas are often oygeer locce npr Cah tin midbrain on ute fondo dy ‘Bah on wad oes st048)-+ oflen owed ty gape "Dilatation of one pupil: CNL compression -> neurosurgical emergency + Homers syndrome (ptosis + miosis: hypothalamic damage + lateral mid-point act pupils (Le, normal pupils): metabll comes + Bilateral ihtfixed Gated aus one ofthe rai deat ca * Bilateral pinpoint, lighted pups: pontine nury = Bilstewal vnidgestthoo Vegeta ce silly dialed tight fired pupils s BS injun Pageaof5 Dieter id-postiontightine-orsightpclted ightined pupils 8S hy © Extraocular movements Oculomotor paresis [Nbsence of blinking in response to visual threat Nystagmus Exophthalmus or enophthalmus Point of interest: ‘* fa patient isin true coma and you lft théir eyelids and let ther go, they wil gradually cover the eyes ‘= Ifa patient isin a hysterical coma and you lift their eyelids, the lids wil rapidly close © Fundi: look for papilloedema and retinal haemorthagé ro-ophthalmic reflexes Oculocephati refiex ‘+ Itis tested by the doll's-eye maneuver ‘+ The eyes are observed while the head is passively rotated from side to side or flexed and extended. + spine injures need to be ruled out before the maneuver is done! + Oculovestibuiar pathways in the brain stem are intact (= reflex is present): eyes move in the opposite direction of head rotation flexion, or extension Oculovestibuiar (cold cori) testing + Indication: f the patient is unconscious and the aculocephalic reflex is absent or the neck i immobilined ‘© First confirm tympanic membrane integrity -> elevate patients head 30° - irrigate the external auditory canal with 50 mL of ice water over a 30-sec period ‘© Nystagmus away from the Irigated + both eyes deviate toward the irigated ear - Intact brainstem ‘+ Respiratory patterns © Periodic cycling of breathing (Cheyne-Stokes or Biot respiration) may indicate dysfunction of both hemispheres or of the diencephalon (BS is intact) (© Hyperventiation (central neurogenic hyperventilation) with respiratory rates of > 40 breaths/min may indicate ‘midbrain or upper pontine dysfunction ‘© An inspiratory gasp with respiratory pauses of about 3 sec after full inspiration (apneustic breathing) typically Indicates pontine or medullary lesions; this type of breathing often progresses to respiratory arrest (© Cushing flex: hypertension + bradycardia + irregular breathing -> ICP ‘© Investigations © Blood and urine Drugs screen (ex: salicylates, diazepam, narcotics, etc) Biochemistry urea, electrolytes, glucose, calcium, etc} Metabolic and endocrine studies Blood cultures (© Imaging -> CT or MRI ©/ CSF examination é eG Page 4of5 ‘toe Definition: A condition of complete unawareness of the self and the environment accompanied by sleep-wake ston. disoicdeas cycles with > Yawake but not aware" + Follows comatose state © Cause: ifVePibl Wate TO OFLERend hemispheres BLT intact brainstem function eres BUT aie alate function, With complete or partial preservation of hypothalamic and brainstem autonomic function © Prognosis: average life expectancy is 2-5 years ee Pec fe, cohneal «flew + bag wfloy & Ayroe tee + Braiaeaiy otto flies Seeseubatae oO tir Ot spdnlontaus bse! eg? a flea. © There's no clincal evidence of bain function upon physical examination [00 response to poin and no rari nerve reflexes) «© GRRTRGABERY - ceretromeduospinalccomection ©The patents aware but cannot move or communicate verboly de to complete paralysis of neat voluntary inthe ae theeves. © Cause: ‘THE DIFFERENCE BETWEEN COMA AND SLEEP, ‘¢ Sleeping persons respond to unaccustomed stimull Sleeping persons are capable of mental activity (dreams) + Sleeping persons can be roused to normal consciousness + Cerebral oxygen uptake does not decrease during sleep as it often does in coma K. MawaGMeNT + Immeckate stabization (ABC) + frequent monitoring of vital functions + supportive measures, including, when necessary, control of ICP + Admission to an icu + Treatment of underlying disorder + [longterm ese) © [ Skincare} turning to avoid pressure sores and pressure palsies), removal of jewellery (© [Oral hygiene} mouthwashes, suction Eyecare: prevention of corneal damage (is taping, rigation co [fluids intragastric ov Caloriesiguid diethrough afin intraga Sphincters{eathet tube, 3000 keal dally ionvhen essential use Paul's tubing if possible); rectal evacuation PTosl Aecavens | o | Recovery NCS. € 5 F Neoe lave clate foruronout NCS | ‘ { fea tain |_, an ¢ \s oe nly 1 pemounnt Verstanye stale wg “E LeSnain ctoat ln FHCS = mintucally cowrclous qd Pages of, © DEFINITION: a svionme son NE) 4. Diabetic ‘© Hipetelveemias hyperosmolar non-ketotie coma; Ketoacidosis 2. on imbalance: natremias,calcemias 3. Renal failure: uremic encephalopathy Vines as verte See ee (© Hepatic encephalopathy ~ Srociomntsiny: (© Wernicke encephalopathy + Bealyler. 48 NA, 2nd ‘© Thyroid storm (hyperthyroid) + Gndocatnt invec we) ae © Aen esis (hyposdrenal) gestae 6, AG imbalance: hypoxla, hypercapnia, severe acidosis = Taxi egy ‘Laren 7 Toxesopy*poeing + cs, ps Hoot gnss ppt @ HYPOGLYCEMIC COMA Pathogenesis: glucose in blood ~ inadequate supply of glucose to the brain -> neurogiycopenia ‘Acute compensatory mechanisms: reduction of insulinsecretion to undetectable levels, and release ‘of glucagon, adrenaline (SS) Prolonged hypoglycemia compensation: ketogenesis Etiology: o> Drugs’ © Sepsis 04 Acute verfallure 1 pucortoeusa’s £ ala cogen shore > Acute ler fallure cone ayes ) omas, LG-1 secreting tumours TANS. + pallee * tnagpioptiol = pepression, aleahol or drug use © Investigations = Linsulin & J C-peptide: alcoho), adrenocortical failure, critically il + Tinsuling J Creptide: excessive insulin injection Cenogtirous souece’) + insulin & 7 C-peptide: insulin secreting tumouss,sufonylureas_ (ev ogenoUe Soueca > © Management 1 AGC. 4 “a Unconscious patient: IV glucose or 20% dextrose + glucagon. ‘Full meal as soon as mental status permits Conscious glucose PO ‘tnx sugae packs, coca coo Page of? DIABETIC COMAS -3 Yor 944.01 128+ PYaleeric +41, SEVERE DIABETIC HYPOGLYCEMIA (insulin overdose) 2, DIABETIC KETOACIDOSIS Ethiology ‘+ "manifestation in an undiagnosed patient ‘Triggers on the diabetic pationt: major trauma/stre: lure of compliance; infection; ischemia Pathogenesis + insulin > 4 uptake of glucose into cells > hyperglycemia + 4 counterregulatory hormones (glucagon, cortisol, catecholamines, GH) -> unrestricted hepatic ‘ucose production > hyperglycemia + Hyperglycemia > osmoti diuresis > dehydration and electrolyte disturbance * Dehydration + hypovolemia > hypoperfusion > * lactic acid > metabolic acidosis * Without treatment: unconsciousness, from a combination of severe hyperglycemia, dehydration, shock, and exhaustion Clinical features ‘+ From hyperglycemia: polyuria, polipsia, weightloss, muscle pain & weakness + From dehydration: severe abdominal pain, gradual drowsiness = From ketoacidosis: nausea, vomiting, fruity odour, Kussmeut’ respiration * lf severe: LOC, coma Diagnosis: Arterial blood pl < 7,5 + Serum HCO3 < 15+ Ketonurla ‘Management 0. Immediate resuscitation and emergency measures if patient is stuporous or comatose 4 Replace fud losses: IV isotonic ud (0.9% saline + 20 mmol/L KCL) ‘Slowly administered to avoid cerebral edema 2.Continuous infusion of short-acting insulin = Critical to resolve acidosis, not hyperglycemia = Use only regular insulin = Check serum glucose hourly > fit falls below 200 before acidosis is corrected, add glucose to infusion 3 Potassium replacement + As acidosis is corrected, hypokalemia may develop (insulin promotes K+ Into the cels) + When K 3.55.5 mmol/L add KCUK,PO, to fluid to keep Kin the range 4. carbonate therapy: Only given if pH <7.0[otherwis, there's risk of metabolic alkalosis) ‘+3. HYPEROSMOLAR NON-KETOTIC COMA, In Type 2 dehydrated DM Pathogenesis ‘+ Basal insulin is enough to suppress lipoprotein lipase activity > no ketogenesis "+ Relative insulin deficiency decreases glucose utilization while inducing hepatic glucose production Trigger: dehydration caused by excess diuretics, renal fare, burns, sepsis, drugs (glucocorticoids) = Volume contraction -> shift of fluid from neurons to ECF -> mental obtundation and coma Complications: occlusive events (Ml, stroke, arterial insufficiency) Management * 0. 1mmediate resuscitation and emergency measures i patients stuporaus or comatose 1. F 099% saline Iv, aver 48h) ‘+ 2.Search for precipitating event + A.Rehydration +3. Insulin therapy: ‘© Wait ah before starting Page2 of 7 Use only regular insulin Initially load, then maintain with a lower dose © Ingeneral lower insulin requirement compared to DKA * Prevouty (SSE + Untreated patient orfion-compliance) + (SRR urge, infection, trauma ose of corticosteroid when undergoing any stressful event : © Presentation’ nausea, vomiting, headache, irritability, letharey seizures, coma, or even death ‘When hyponatremia is accompanied by disturbances in total body Na content, signs of ECF volume depletion or overload also occur CChronie = asymptomatic ‘Management: ‘+ Asymptomatic: slow Nat Infusion of maximally <12mmolin the frst 24h ‘+ Symptomatic: 3% saline IV immediately at a rate of 1 mmol/L per hour until neurologic symptoms are controlled > followed by a rate of 0.5 mmol/L per hour (© Aaute hypernatremia is caused by an excess of water relative to solute (primary gain in Na* or excess loss 0, water) > ae) Gain _in sodium can result from: hyperaldosteronism, Cushing's syndrome, or excessive hypertonic saline or sodium bicarbonate administration Loss of free water can result from gastrointestinal losses or renal excretion (eg, osmotic diuresis or clabetes insipidus} CE: a major symptom is thirst ‘Acute: cerebral pontine myelinolysis> confusion, neuromuscular excitability, selzures, and coma ‘Management: slow replacement of intravascular volume and free water orally or intravenously (©The magnitude of the potassium gradient across cell membranes determines excitability of nerve and muscle (© Evaluation of serum potassium must consider the effects of changes in serum Ph: when serum pH falls, serum potassium rses because potassium shifts from the cellular to the vascular space; and vice-versa © Hyperkalemia Severe if>7mmol/L ‘most commonly seen in patients with end-stage renal disease CCF: weakness, ascending paralysis, and respiratory failure Management ‘© Shift potassium into cells: Glucose plus insulin, Nebulized albuterol, Calcium chloride + Promote potassium excretion: diuretics, enemas, alysis © Hypokalemia ‘Most common causes: + Gloss (diarrhea, laxatives) + Renal loss (hyperaldosteronism, severe hyperglycemia, potessium-depleting diuretics, carbenicilin, sodium pentcilin, amphotericin B) ‘¢ Intracellular shift alkalosis or arse in pH) ‘+ Malnutrition ‘The myocardium is extremely sensitive to the effects of hypokalemia, particularly if the patient has coronary artery disease ori taking a digitalis derivative Page dof 7

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