Absite Topic Review

Nir Hus, MD, PhD.

04/10/23

Topics

1) Postop Parotitis. 2) SVR – Hypo olemic shock. 3) Prevent / risk factors ARDS .

Parotitis Can occur in the surgical patient and identified during the

postoperative period. Particularly in elderly Dehydrated individuals.

Therapy should be directed toward Rehydration Enhancing salivation Ensuring that no mechanical obstruction of the duct of Stensen

is present Obtaining stains and cultures Administering antibiotics directed against S. aureus, which is the

most common offending organism. In ICU patients who are often colonized with gram-negative

bacteria, the possibility of gram-negative bacterial parotitis should be considered and appropriate empiric therapy used.

I&D

SVR – Hypovolemic shock.

Q: In a hypotensive patient in the intensive care unit, the finding most useful in the diagnosis of sepsis is a

A. CVP of 8 cms H2O

B. Cardiac index of 2.5 L/min/m2

PH of 7.38 Systemic vascular resistance of 500 dynes.sec/cm. M2

Pulse rate of 120/min

SVR – Hypovolemic shock.

Answer: D. Unlike other forms of shock, patients with septic shock are

normovolemic with reasonable filling pressures. The cardiac output is increased secondary to the hyperdynamic

state induced by the sepsis. The peripheral resistance is low and produces the paradoxical

warm shock with pink dry extremities. A low systemic vascular resistance is therefore most useful

in establishing the diagnosis. Tachycardia is a nonspecific finding and does not suggest any

specific etiology

Adult respiratory distress syndrome:

Q: ARDS,

A. is associated with and increase in FRC above closing volume

B. results in ventilation and perfusion mismatch and shunting

C. is improved by an increase in FiO2 D. is accompanied by and increase in the number of

type I alveolar cells E. is characterized by the accumulation of protein rich

exudate

ARDS

By definition, ARDS is the clinical situation in which the patient is incapable of maintaining adequate: Oxygenation Ventilation Tissue delivery Or some combination of these defects.

The cause of this failure may be single and identifiable, such as pneumonia. Alternatively, it may represent the end point of a poorly understood pathway with a

common final denominator of lung damage and subsequent decompensation of oxygenation and ventilation.

The most widely accepted definition of ARDS is the syndrome that includes 1. Lung injury, acute in nature, 2. Bilateral infiltrates on frontal chest radiograph, 3. PaO 2/FIO 2 less than 200, 4. Pulmonary-capillary wedge pressure less than 19 mmHg with no evidence of congestive

heart failure.

ARDS – cont.

These same findings when associated with a PaO2/FIO2 less than 300 are defined as “acute lung injury” (ALI).

The signature of ARDS is a ventilation/perfusion mismatch. Alveolar hypoventilation occurs because of collapse, expansion of the alveolar

membrane, or presence of exudate and fluid within the alveolar spaces that are still available for perfusion.

This “alveolar block,” when combined with changes in perfusion relationships, results in the increased hypoxemia manifested as a shunt as well as increased dead space.

There is actually a decrease in FRC as alveoli are lost and this is therefore not helped by an increase in FIO2.

The management of ARDS is based in recruitment of alveoli by increase in PEEP.

There is a decrease in the number type I alveoli cells as these are damaged by the ARDS process.

There is an accumulation of fluid within the alveoli but ventilation/perfusion mismatch seems to be a better answer. (Swartz ch 11 (ARDS)) - ANSWER – B