Recognizing the Critically Ill Patient Andrew Wormsbecker PGY5 Critical Care Medicine Disclosures y none Objectives y Use a systematic assessment approach to identify underlying physiologic problem(s) and their causes to direct initial treatment of seriously ill patients y Elicit patient features on history that indicate increased risk for deterioration y Perform initial examination and interpret vitals and other findings as they relate to identification of organ dysfunction or limited reserves y Choose and interpret high yield initial investigations y Plan follow up assessment (what will be done, who will do it, and when) based on your expected response to treatment y Distinguish acute from chronic disease presentation y Identify various healthcare providers you can call upon to help in the care of your patient. Additional Objectives y Approach to shock y Lactic Acidosis Intro y Many patients demonstrate concerning historical symptoms or physiologic signs hours before cardiopulmonary arrest y Young, fit patients have large compensatory reserves y Immunosuppressed patients may not mount robust responses which may mask signs of illness “How sick is this patient?” y “Spidy sense” and clinical experience will help guide you y You have a senior, and a staff with more of this experience y An organized approach will help you build this experience and pattern recognition y The CA system has taken away a lot of the “on-call emergencies” at VGH and SPH y Try and tag along if you aren’t slammed Case y 54M, HIV+ not on treatment presents with SOB, mild pleuritic chest pain and a new RLL infiltrate y Sr “triages” patient and then gets called away so sends you to see as the IM Jr because patient looks pretty sick y All: none y Meds: ventolin, flovent, aspirin y PHx: 1 intubation for asthma in past, HIV for 5 years from past IVDU, no treatment, CD4 50 y 2 days of chills, “fever”, SOB, productive cough of green sputum, worse today, hard to catch breath, no immunizations y OE: y 120/70, 125, 26, 89% on HFFM, 38.5 y Dissheveled, looks “sick” y Mildly drowsy, easily roused, GCS 13 (E3, V4, M6) y CVS: JVP @ sternal angle, flow murmur, normal S1S2 y Resp: increased acc muscles, tracheal tugging, increased tactile fremitus RLL, expiratory wheeze throughout, RLL coarse crackles and bronchial breath sounds y Abdo: unremarkable y Skin: mottling of knees y Fingers: mild acrocyanosis y Inv: y WBC 13 with N 12, Hgb 125, Plt 120 y Electrolytes normal y Cr 125 (baseline 50) y HCO3 16 y Lactate 4 y ABG: 7.27/31/70/17/-6 on ~40% Fi02 y CXR: RLL opacity y ECG: sinus tachycardia Can you write-down what indicates critical illness Approach to the Sick Patient y “ABC, MOVIE” y Airway, Breathing, Circulation y Monitor, Oxygen, Vital Signs, IV, Exposure/draping/lighting

y Should be first words out of your mouth on any OSCE acute medicine physical exam or oral scenario

y Akin to “Primary survey” from trauma y THIS COMES BEFORE YOUR HISTORY DESPITE WHAT THE BOOK SAYS ?What does this actually mean? y Airway y -is the patient protecting their away y Hint: if they can talk to you, they are protecting and you can move on y If unsure, ask a question y If not: Ask for help, assess for airway obstruction (foreign body, signs of stridor), noisy breathing, grunting, cyanosis y level of consciousness (GCS – “less than 8=intubate) y Breathing (not your complete resp exam!) y -look, listen, feel y If they are talking, probably not a huge problem y Look at symmetry, pattern, rate, accessory muscle use y Many potential locations of disorder y CNS- decreased drive y Cardiac- ischemia, valvulopathy, rhythm, pump failure y Bellows- neuromuscular, chest wall y Airway y Parenchyma y Vascular y Pleura y Systemic conditions – anemia, sepsis, liver failure, drugs Breathing Patterns y Bradypnea: sedative-hypnotics (Benzos, EtOH), narcotics, encephalopathy y Tachypnea: acidosis, sepsis, sympathomimetics, ASA y Biot: ataxic respirations y Severe brain injury/medullary injury y Cheyne-Stokes: apneas followed by hypernpneas that then decrease to apnea y Altered “loop-gain” response to CO2 y Think CHF, bihemispheric or brainstem injury y Kussmaul: deep, labored, gasping breaths that typically follow initial tachynpea y Compensatory hyperventilation for severe acidosis y *think DKA, lactic acidosis y Circulation: y HR, BP, orthostatics y *skin warmth, mottling y Assess pulses for rate, volume, regularity, symmetry y Can actually assess pulsus by palpation (but should do BP if concerned)

y May relate to primary cardiovascular problem or secondary to metabolic issues, sepsis, hypoxemia, drugs Historical Features y Classically >90% diagnosis made on history y In critically ill, patient may not give history! y Collateral: nurses, care aides, family, friends, EHS, other consult notes, chart, etc Historical Features y Rapid History: y Signs/symptoms y Allergies y Medications y Past Hx y Last meal y Events surrounding

y OPQRST of issue y Symptoms will usually direct toward organ-specific history and approach – ie chest pain, dyspnea, altered mental status y -separate talks y Attempt to distinguish acute from chronic dysfunction, assess for reversible causes y Eg: COPD patient with high CO2 – look at the compensation to see if acute or chronic y Look at previous notes, dictations, dig for collateral y Focus on what has changed from their baseline People to worry about: y Emergency admission- limited info y Advanced age – comorbidities, limited reserve y Severe coexisting illnesses – juggling problems, limited reserve y Severe physiologic abnormalities – limited reserve, refractory to therapy y Need/recent major surgery y Severe bleed, need for massive transfusion y Deterioration on repeat assessment/fail to respond to treatment y Immunodeficiency y Combinations of above y SIRS response Other people I worry about y Asthmatics/COPDer’s with past ICU, intubation y Submassive PE’s y Anyone who’s pregnant, especially with respiratory illness y Young septic patients y Polysubstance overdose, long-acting drugs (like methadone!) y Severe valvular abnormalities or pulmonary hypertension y Elevated lactate with no great explanation y DKA y Severe hyponatremia y The pneumonia patient on BiPap y Unexplained metabolic acidosis Examination y After your screening ABC’s and vitals move on to “complete focused physical exam” focusing on the suspected organ system involved y “secondary survey” y Neuro: CN, screening motor and sensory, reflexes y Cardiac: IPPA, peripheral pulses y Resp: IPPA y Abdo: IPPA, always lay hand on abdomen y Don’t neglect the skin/integument y Dry, wet, think, thick, edematous, bruised, cyanosis, rashes y Nails: clubbing, splinters y Eyes: icterus, pale conjuctiva Investigations y CBC with dif, lytes, urea, Cr y WBC with left shift may be sign of infection y Metabolic acidosis, AG may be early sign of critical illness y Pay attention to unexplained low HCO3 y ABG y Trop, CK, LACTATE y CXR y ECG Put it all together y Recognize patterns from history, physical, investigations SIRS y Systemic inflammatory response syndrome y May be a clue of sepsis y At least 2 of: y HR> 90 y Temp <36 or >38 y RR > 20 or PaCO2 <32 y WBC <4, >12, or >10% bands Management y Depends on etiology y Ensure large bore IV access (>18G x 2) y Early aggressive fluids in septic and hypovolemic patients y Early antibiotics in patients with SIRS/sepsis y 8%/hr decreased mortality after onset of low BP y Supplemental O2 y Call for help! Reassess y Critically Ill patient will require much more time y Not a consult you can bang out then see with staff in the morning y Frequent reassessment y After each intervention assess the response y If not respond ASK FOR HELP Who can I call?! y 1) your Senior y 2) your staff – yes you can call them! It doesn’t matter if they are sleeping y 3) Resp Therapist- can assist with high flow O2, BiPap, ABG’s y 4) VGH: CCOT – can actually be nurse triggered as well y *THIS IS WHAT CCOT IS FOR, THERE IS AN INTENSIVIST ON THE TEAM DURING THE DAY y 4) SPH and RCH: no CCOT at present y 5) HAU/ICU Consult y **if your patient is sick enough that they need critical care your staff needs to know about it y You are operating under their name, they are ultimately responsible and are supposed to supervise you Who needs ICU?

Jones et al. Intensive Care Med. 2015 Shock Definition y “state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization” y DOES NOT necessarily = hypotension y “cryptic shock” or compensated shock y Compensatory tachycardia, vasoconstriction y “normal BP” may be hypotension for that individual who has shifted their auto-regulation to the right

Shoemaker. New Horiz. 1996 Holmes. Clin Chest Med. 2003 Gaieski. Uptodate. 2015. ICU Equation y DO2= CO X O2 carry capacity y DO2= CO X (HgbX1.34 X SaO2 + 0.0031PaO2) y CO= HR X SV y SV depends on PL, AL, contractility y DO2 ~ VO2 y When DO2 drops below critical value (anaerobic threshold) shift from TCA cycle to anaerobic metabolism - >lactate production

Marino. The ICU Book. 2014

Types of Shock y 3 main types: y Distributive/Vasodilatory y Hypovolemic y Cardiogenic/Obstructive

-Can also think of as “warm” – vasodilatory problem, and “cold” – cardiac output problem -in reality, often mixed Shock Type Preload SVR CO PCWP/CXR (CVP/JVP)* (warm/cold) Distributive low Low/warm high Low/clear Hypovolemic low High/cold Low/normal Low/clear Cardiogenic high High/cold low High/wet Obstructive high High/cold Low *PE-low/clear *TPTX- low/clear *tamponade- high/wet Hypotension y It’s all math!- sort of y BP = CO X SVR y CO= HR X SV y SV determined by PL, AL, Contractility 4 questions y 1) Warm or Cold? – feel leg y 2) Empty or full? – JVP/CVP/Ultrasound IVC y 3) Lungs wet or dry? y 4) From above answers which subtype ->differential for that subtype Distributive/Vasodilatory y SEPSIS – another talk y Adrenal Insufficiency, thyroid storm y Neurogenic (esp T1-T5 injuries) y Reperfusion injury/post-resuscitation/post cardiac arrest y Anaphylaxis y Fat, air, amniotic fluid embolus y Liver failure y SIRS syndromes- pancreatitis, idiopathic capillary leak y Burns, truama, crush injury y Drugs – cyanide, long acting opiates, serotonin syndrome, TCA’s Hypovolemic y Hemorrhage y GI losses - Severe diarrhea, vomitting y Skin – toxic shock, TENS, burns, etc y Renal – hypoaldo, salt wasting, osmotic diuresis (DKA, HHS, etc) y Third spacing- burns, pancreatitis, bowel obstruction, post-op Cardiogenic y Heart is simple! It’s a pump! y Wiring – rhythm problem (brady/tachy) y Plumbing – CAD – MI, vasospasm, cocaine y Mechanical – valve failure – MR, MS, AI, AS, HOCM, septal rupture y Pump- CHF, cardiomyopathy, constriction, diastolic dysfunction, HTN, myocarditis Obstructive y Low cardiac output state from obstruction to filling right or left heart y Tension Pneumothorax y Pulmonary Embolism y Cardiac Tamponade y Constrictive Pericarditis y Severe Pulm HTN y Right Heart Failure y Abdo Compartment Syndrome y IVC tumor Unusual Causes when things don’t make sense y I keep this list on my phone y Extreme hyper/hypothyroid y CO y Cyanide poisoning (usually from fires, not poisonings) y HLH y Mastocytosis y Scromboid y BeriBeri y Sheehan’s/Pit failure y Pheo y Tetanus y Serotonin Sx y GBS y Toxic shock syndrome- staph or strep y Drugs y Profound electrolyte abnormalities- hypoCa, hypoPO4 y Severe acidosis – catecholamine unresponsiveness y Anatomical defect Shock with relative bradycardia y Cardiac ischemia (RCA/LCx lesions) y Salmonella sepsis, viral infections, CNS infections y Drugs: 2B’s, 3C’s and a D y BB, Barbiturates y CCB, Clonidine, cholinergics y Dig Markers of shock y Vitals: hypotension (and look at pulse pressure, DBP), tachycardia (rarely bradycardia), tachypnea (to compensate for acidosis), fever (infectious etiology) y Exam: altered LOC, JVP/CVP, heart failure, skin mottling, urine output y Labs: Lactate, elevated coags, low platelets, elevated bili, elevated ALT/AST, elevated Cr Mottling y Classic marker of microcirculatory dysfunction y One study of 60 septic shock patients showed that the size of knee mottling, urine output and lactate were associated with mortality whereas traditional resuscitation guides (CVP, MAP, CO) were not

Ait-Oufella et al. Intensive Care Med .2011 Lactic Acidosis y 3 types y Type A: hypoperfusion causing anaerobic metabolism y Type B: non-hypoperfusion, redox state alterations, decreased clearance, etc y Type D: D-lactate (not measured by our labs) – may see unexplained metabolic acidosis in patient with previous short gut/jejenoileal bypass/small bowel resection Lactate Production y Byproduct of glycolysis y Pyruvate + NADH Æ Lactate + NAD+ y In states of anaerobic metabolism pyruvate cannot enter TCA cycle and thus produces lactate y Altered “Redox” state drives pyruvate to lactate y Eg: chronic EtOH – alcohol dehydrogenase uses NAD+ as cofactor resulting in NAD+ deficient state Type A Lactic Acidosis y Hypoperfusion y O2 demands exceed delivery y Microcirculatory > macrocirculatory dysfunction y Find cause: hypovolemia, sepsis, CHF, post arrest, etc Type B y Altered Redox State y Chronic alcohol/AKA y DKA y Epinephrine/catecholamines y Hypothermic shivering y Strenuous exercise y Post seizure y Mitochondrial dysfunction (drugs, sepsis, toxins, genetic like MELAS) y Impaired pyruvate usage y Reye’s syndrome y Diabetes y congenital y Increased pyruvate production y Glycogen storage diseases y Resp Alkalosis y Beta Agonists y Malignancy – esp hematologic or large tumor burden y Increased metabolism, rapid growth y Decreased clearance y LIVER FAILURE – 70% lactate clearance y Renal failure - <20% of lactate clearance y Drugs y Metformin y Stavudine and zidovudine y Propofol y Ethylene Glycol y Cyanide, toluene, arsenic y linezolid

McCullough. UpToDate 2015 De Backer. Intensive Care Med 2003 Lactate Clearance y Lactate clearance >10% at 2 hours is a marker of organ perfusion and improving circulation in sepsis y Failure to clear lactate associated with increased mortality y As good as mixed venous in a 300 person study y *3 recent trials do not support mixed venous monitoring y You will hear more about this in your sepsis talk

Jones. JAMA 2010 Back to our case What are concerning? y All: none y Meds: ventolin, flovent, aspirin y PHx: 1 intubation for asthma in past, HIV for 5 years from past IVDU, no treatment, CD4 50 y 2 days of chills, “fever”, SOB, productive cough of green sputum, worse today, hard to catch breath, no immunizations y OE: y 120/70, 125, 26, 89% on HFFM, 38.5 y Dissheveled, looks “sick” y Mildly drowsy, easily roused, GCS 13 (E3, V4, M6) y CVS: JVP @ sternal angle, flow murmur, normal S1S2 y Resp: increased acc muscles, tracheal tugging, increased tactile fremitus RLL, expiratory wheeze throughout, RLL coarse crackles and bronchial breath sounds y Abdo: unremarkable y Skin: mottling of knees y Fingers: mild acrocyanosis y Inv: y WBC 13 with N 12, Hgb 125, Plt 120 y Electrolytes normal y Cr 125 (baseline 50) y HCO3 16 y Lactate 4 y ABG: 7.27/31/70/17/-6 on ~40% Fi02 y CXR: RLL opacity y ECG: sinus tachycardia Case Resolution y You start patient on CAP antibiotics, PJP coverage y BP decreases, you give 2L crystalloid with improved BP, lactate clearance y Oxygenation gets worse, starts desatting y ICU called, come intubate patient, place on pressors and take to unit