hypotension and respiratory distress

7/31/2019 Hypotension and Respiratory Distress

1/15

Mariposa Wolford

Morning ReportHypotension and fever in an 18 year female


2/15

ICU nights

18 y/o female with BPs low after nearly 3L NS

Diagnosis of AML, s/p Induction II, CNS negative,

MRD negative

Recent course of chemo with Ara C finished on7/25. Currently neutropenic and has had low plts

Had high fevers with her chemo

PMHx includes allergic rhinitis and PCOS, on

OCPs. Diagnosed with AML


3/15

Patient presentation T 39.9 HR 124 BP 95/31 RR 18 on 0.5LPM O2

with sats 97%

Wt 64kg

GEN: pt smiling, NAD, alopecia 2/2 chemo, AOx3

HEENT: NCAT, EOMI, PERRL, MMM, noexudates in throat

CV: Tachycardic with no m/r/g. Bounding pulsesin all 4 extremities. CRT 2s

CHEST: CTAB. With mildly increased WOB. Nowheezing, no crackles.

ABD: S/NT/ND. No HSM.


4/15

Over the next few days

Increasing respiratory distress and oxygen needprompting HFNC after increased NC

Trial back on NC resulted in desats to mid 80s

CXR showing mild ill defined opacification inlower lungs

Patient with diarrhea, continued high fevers into

the 40s and increasing fatigue.

Mixed venous sats decreasing


5/15

Differential diagnosis Pulmonary hemorrhage Bacterial sepsis

Fat embolism syndrome

Acute respiratory distress

Transfusion associated lung injury (TRALI)

Acute eosinophilic pneumonia Acute hypersensitivity pneumonitis

Leukemic infiltration

Pneumocystic jiroveci pneumonia

Bacterial or viral pneumonia

Multi organ failure associated with sepsis Respiratory failure

Toxic shock syndrome

Tumor lysis syndrome


6/15

Other info on our pt Blood culture from 8/2 positive for viridans Strep

On Vancomycin and Ceftazidime, then Cefepime

Mixed venous saturations about 70->59->74->69

Switched to Bipap 12/8, then 14/10 before intubation on8/6 am since she had coughing spells despite increasedBipap settings

Wt was up from about 64kg to about 68.9 after fluids andblood pdts. Went on lasix drip, needed bld pts, wasfebrile/shivering so we paralyzed and sedated her


7/15

Course

Had blood from ETT

LS had left lung collapse on 8/8

Bronchoscopy showed excessive secretions

Given pulmozyme On VDR ventilator for 3 days, then got

subcutaneous air in limbs

Switched back to conventional ventilator

Was intubated for 12 total days!


8/15

ARDS Acute resp failure & refractory hypoxemia 2/2

significant lung injury

CXR w bilateral opacities. Lungs are non-compliant

Severity of hypoxemia determines severity of ARDS

using arterial oxygen tension to fraction of inspired

oxygen PaO2/FiO2

>200 but < or = to 300, MILD

>100 but < or = to 200, MODERATE

< or = to 100, SEVERE


9/15

ARDS continued

Lung damage increased alveolar-capillarypermeability influx of interstitial & intra-alveolar

fluid.

Surfactant is diluted and its production decreased

Point on pressure-volume PV loop w/ lower

inflection point


10/15

Pathophysiology of ARDS


11/15

ARDS Histology shows diffuse alveolar damage.

InfectionSepsis

Diffuse pulmonary

infections*

Gastric aspiration*

Chemical InjuryHeroin or methadone OD

Acetylsalicyclic acid

Barbituate OD

Paraquat

CardiopulmonaryBypass

Hypersensitivity

ReactionsOrganic SolventsDrugs

Physical/InjuryMechanical trauma/ inc

head injuries

Pulmonary contusions

Near-drowning

Fractures with fat

embolism

Burns

Ionizing radiation

Hematologic ConditionsMultiple transfusions

DIC

Pancreatitis

Uremia

Inhaled IrritantsOxygen toxicity

Smoke

Irritant gases and

chemicals


12/15

Oxygen delivery: how much oxygen

delivered to tissues in a minute

DO2 = CO x CaO2

CaO2 = arterial oxygen content

= amount of O2 bound to Hgb plus amount of O2dissolved in arterial blood

=(Hb x SaO2 x 1.34ml O2/g Hgb) + 0.003ml x PaO2

SaO2 is the arterial oxyhemoglobin concentrationand PaO2 is the arterial oxygen tension.


13/15

Outcomes Mortality for ARDS 26-58% by one estimate.

Common causes in Peds: drowning, sepsis & shock

Cause of death is usually the underlying cause andnot respiratory failure

Some prognostic factors include: Younger patients do better

Milder cases of ARDS do better Large positive fluid balance do worse Recently transfused pts (pRBCs) did worse


14/15

ARDS outcomes long term

Survivors frequently have long term decrease inexercise tolerance/endurance

80% of pts in one study had reduced diffusing

capacity, regardess of H or LTV trtmt

A better functional outcome at one year correlates

with the absence of steroid treatment, absence of

illness acquired during the ICU stay, and rapid

resolution of multiple organ failure and lung injury


15/15

References Pediatric ICU Blueprint, Schwartz, MD. 2007.

Pulmonary function and health-related quality of life in survivors of acute

respiratory distress syndrome.Orme J Jr, Romney JS, Hopkins RO,

Pope D, Chan KJ, Thomsen G, Crapo RO, Weaver LK. Am J Respir Crit

Care Med. 2003;167(5):690.

Robbins Pathologic Basis of Disease, 7th Ed.

UpToDate: Acute respiratory distress syndrome: Clinical features and

diagnosis. Last updated Oct 5, 2012.

UpToDate:Acute respiratory distress syndrome: Prognosis and

outcomes. Last updated July 3, 2012

hypotension and respiratory distress

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