management of life threatening disease in orl

8/2/2019 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

management of life threatening disease in orl

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