management of life threatening disease in orl
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Management of lifethreatening medical
complication in ORLBy Dr Tshering Sherpa
ORL & HNS departmentBMCH
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Hypovolumic shock
Physician read , surgeon treat the hypovolemicshock
Cardiac output=stroke volume x heart rate
Stroke volume depend upon preload (ventricularfilling)
Cardiac output=major determinant of tissueperfusion
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shock
Decreased tissue perfusion
Cellular dysfunction
production and release of damage-associated molecular patterns (DAMPs or
"danger signals") and inflammatorymediators
Further decreased perfusion
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Mild (
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Severe (>40% Blood Volume)Same plus
Homodynamic instabilityMarked tachycardia
Hypotension
Mental status deteriorationInitial heamatocrit do not change until there is
compensatory fluid shift or exogenous fluid isgiven
Plasma loss cause hemoconcentration and freewater loss cause hypernatrimia-this is thefeature of hypovolemic shock
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Treatment of shock
Starling s Law-stock volume and cardiacoutput increases with increase in preload
Volume resuscitation with isotonic salineor ringer lactate
Colloid use has higher mortality in trauma
patient The infusion of 23 L of salt solution over
2030 min should restore normal
hemodynamic parameters..
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blood transfusion-
continue blood loss with Hb declining7
Restrictive blood transfusion-increase survival
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septic shock
sepsis
SIRS that has a proven or suspected microbialetiology
Microbial invasion of the bloodstream is notessential, since local inflammation can also elicitdistant organ dysfunction and hypotension.
Decrease in peripheral vascular resistancedespite increased levels of vasopressorcatecholamines hall mark of septic shock
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Septic Shock-definition
Sepsis with hypotension (arterial bloodpressure
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Defination
Refractory Septic shock-Septic shockthat lasts for >1 h and does not respond to fluidor pressor administration
Systemic inflammatory responsesyndrome (SIRS) -Two or more of the followingconditions:
(1) fever (oral temperature >38C) or hypothermia(24 breaths/min);
(3) tachycardia (heart rate >90 beats/min);
(4) leukocytosis (>12,000/ L), leucopenia (10% bands; may have a noninfectious etiology
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Treatment of septic shock
Antimicrobial AgentsImmunocompetent adult
1 imipenem-cilastatin (0.5 g q6h) or meropenem (1 g
q8h) or cefepime (2 g q8h)2 piperacillin tazobactam (3.375 g q4h) plus tobramycin
(57 mg/kg q24h).
Neutropenia (
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Removal of the Source of Infection
Metabolic Support-improve tissue oxygen utilization
-measurement of arterial blood pressure,
-monitoring of parameters such as mentation, urine output, andskin perfusion.
-Indirect indices of oxygen delivery and consumption, such ascentral venous oxygen saturation
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Homodynamic support Hypotension-start 12 L of normal saline over 12 h To avoid pulmonary edema, the central venous pressure should be
maintained at 812 cmH2O. The urine output rate should be kept at >0.5 mL/kg per hour bycontinuing fluid administration;
a diuretic such as furosemide may be used if needed. In about one-third of patients, hypotension and organ
hypoperfusion respond to fluid resuscitation;
a reasonable goal is to maintain a mean arterial blood pressure of>65 mmHg (systolic pressure >90 mmHg). Titrated doses of norepinephrine or dopamine should be
administered through a central catheter. If myocardial dysfunctionproduces elevated cardiac filling pressures and low cardiac output,inotropic therapy with dobutamine is recommended.
If not respond to fluid menagement start hydrocortisone 50mg i/v 6hry if clinical improvement occurs over 2448 h, most expertswould continue hydrocortisone therapy for 57 days before slowlytapering and discontinuing it.
Ventilator therapy is indicated for progressive hypoxemia,hypercapnia, neurologic deterioration, or respiratory muscle failure.
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Thyrotoxic crisis, or thyroid storm,
Is rare and presents as a life-threatening exacerbation of hyperthyroidism,
usually precipitated by acute illness (e.g., stroke, infection, trauma, diabeticketoacidosis), surgery (especially on the thyroid), or radioiodine treatment of apatient with partially treated or untreated hyperthyroidism.
propylthiouracil (600 mg loading dose and 200300 mg every 6 h) orally ornasogastric tube or per rectum;
One hour after-A saturated solution of potassium iodide (5 drops SSKI every 6 h), or ipodate or iopanoic acid (500 mg per 12
h), orally. (Sodium iodide, 0.25 g IV every 6 h, is an alternative but is not generally available.)
Propranolol (4060 mg PO every 4 h; or 2 mg IV every 4 h).
dexamethasone, 2 mg every 6 h),
antibiotics if infection is present, cooling, oxygen, and intravenous fluids.
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Acid base disorder
Important organ are Lung and Kidney Lung excrete Carbon di oxide
Kidney reabsorb or excrete bicarbonate Effect on ph summaries by Kassirer
equation-
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Arterial Blood Gas Interpretation
Normals: pH 7.35-7.45
pCO2 35-45 pO2 80-100 HCO3 22-26(For calculations assume normal pCO2 40
and HCO3 24)
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Metabolic acidosisanion gap =
Normal anion gap
Hyperchleromic
Loss of bicarbonate-Fistula, diarrhea
Renal-renal tubular
acidosis
High anion gap
StarvationDKA
Failure of acid excretion
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Compensation
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Metabolic Alkalosis
Chloride responsive
Vomiting,
NG tube drainage ,Diuretics
Massive blood
transfusionGlucose ingestion afterstarvation
ChlorideUnresponsive
Excess mineralcorticoidschronic steroids
Cushings Syndrome
Hypokalemia
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Respiratory Acidosis
Acute
Airway obstruction
Neuromuscular paralysis
Chronic
COPD
Ca larynxTracheal stenosis
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RESPIRATORY ALKALOSIS
Central Peripheral
Anxiety Pulmonary embolism
Head trauma Pulmonary edema
Brain tumors orvascular accidents Interstitial lung disease (early)
Salicylates Pneumonia
Fever Altitude
PainPregnancy Iatrogenic
Mechanical ventilation
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Hyponatremia-depletional
Hypertonic Saline (3%) should only be used insymptomatic hyponatremia if the patient is (1) acutelycomatose, and/or is seizing and has sodium valuebelow 120.
Give 100 cc of Hypertonic Saline over 10 minutesfor seizures; follow with a second 100 cc overthe next 50 minutes if patient is still unstable (200 cc
over 1 hour is maximum)
Correct patients at a maximum of 0.5 meq/hr or
no more than 10 - 12 meq/day. (Note: mayexceed 0.5/hr if using hypertonic saline; But cannot exceed 10 -12/day).
Never Correct Patients Sodium by more than 10-12meq/day. Aim for 0.5 meq/hr unless seizing or
comatose.
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Dilutional Hyponatremia: Renal dysfunction with intake of hypotonic
fluids
Excessive sweating increased thirst intake of excessive amounts of pure water
Syndrome of Inappropriate ADH (SIADH) or
oliguric renal failure, severe congestive heartfailure, cirrhosis all lead to:
Impaired renal excretion of water
Hyperglycemia attracts water
Tx limit water intake or discontinue meds
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Hypokalemia
Hypokalemia has many causes, the most commoncauses for patientspresenting to the ED are:
1) Diuretic use2) Malnutrition3) Alcohol Abuse4) Vomiting5) Diarrhea
The two serious complications of hypokalemia are: Cardiac Arrythmias Rhabdomyolysis
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The two serious complications ofhypokalemia are:
Cardiac Arrythmias
Rhabdomyolysis
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Hypokalemia
Serum K+ < 3.5 mEq /L
Always give magnesium with potassium repletion
Total body K deficit is difficult to predict
Always takes more K than you think
About 100 meq per each 0.3 meq falling below normal
Dont give more than 10-20 meq/hr IV;use, PO too!
Beware hypokalemia; replace K aggressively!
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HYPERKALEMIA
Hyperkalemia is the most dangerous acuteelectrolyte abnormality.
The number one cause ofhyperkalemia is hemolysis after (oras) the patient's blood is drawn.
Treat the patient based on laboratoryvalues and ECG changes, and not justlab values
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ECG Changes in hyperkalamia
Sine Wave
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TREATMENT OFHYPERKALEMIA
Step 1: Reverse the deleterious electrical effects of potassium (Trick theCell)
a) 5-10% of CaCl- only if wide QRS
Step 2: Drive potassium into the cell
-2 amps D50 over 5-10 minutes with 10 units of regular insulin IVpush.
-Continuous inhaled beta agonists
-2 amps (1 meq/kg) NaHCO3 over 5-10 minutes-only if acidotic
Step 3: Remove potassium from the body
-NSS at 200 cc/hr and lasix (40 - ? mg) to achieve urine output -approaching 150 cc/hr; only if good renal function; e.g. rhabdomyolysisdue to dehydratuion
-Kayexalate 50 G in sorbitol PO or by enema- Hemodialysis
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Hypercalcemia
Secure ABCs, Consider NGT (bolus salinetill perfusing)
Begin Saline (blocks proximalreabsorption)150-250 cc/hr; not faster Titrate Lasix (follow Intake/Output)hold
lasix till volume repleted
Follow K and Mg values (beware HypoK asyou diurese) Call Internist/Oncologist (let them choose
next drug; usually a biphosphonate
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Hypocalcemia
Diagnosis: Chvosteks sign Trousseaus sign
Treatment IV calcium for acute Oral calcium and vitamin D for chronic
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True hypocalcemia- level of ionized ca
Hypocalcemia- total Ca concentration Alkalosis - binding of ca to protein-directmeasurement is essential
Ca level are effectively by steroid
Vitamin D (40,000 120,000U/d or 1-3 mg/day) & ca >1g/d is usually satisfactory
Oral ca and vit D restore ca-po balance but do
not reverse lower urinary ca reabsorption Hypomagnesemia should be corrected
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Thanks for your attention