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M&m-Hypovolemic Shock
M&m-Hypovolemic Shock
MORTALITY
May 2019
PATIENT’S PROFILE
C. E
69 y.o./ Female/ Married
1 week PTA
Consulted a surgeon and was advised for admission for surgery
Morning PTA
Had her regular dialysis session, purplish discoloration was also noted on her left breast
Admission
At ER: Conscious, coherent, cooperative and not in acute respiratory distress
Vitals: BP 110/80 O2 sat 94% RR 20 HR 81
HISTORY OF PRESENT
ILLNESS
Admission (con’t.)
Started on Piperacillin-Tazobactam 4.5 gms IV, Tygacil 100mg IV, Tramadol 50mg x 1 dose,
Paracetamol 500mg 2 tabs po, Levofloxacin 250 mg IV drip every other day
Maintenance meds were continued: ISMN 30 ½ TAB PO , Clonidine 150 mg 1 tab po, Carvedilol
6.25mg tab OD , Lacidipine 2mg/tab 1 tab OD , Vitamin D BID , Ferrous Sulfate OD , Gabapentin
100mg/ cap OD , Telmisartan 50 OD
Pro-time
Normal Results Normal Results
Patient (11.5-15.5) 20.9
Clotting time (7-15 mins) 13’00”
Control 13.2
Bleeding time (2-8 mins) 8’00”
% Activity (70-100%) 45%
INR (<1.2) 1.77
PREOPERATIVE EVALUATION
ECG: SR, PRWP, NSSTWC
2DED:EF 48% (M-MODE and Simpsons) CLVH with SWMA indicative of CAD with
moderately depressed LVSF with Doppler evidence of grade 2 diastolic dysfunction, dilated
left atrium, aortic sclerosis with mild aortic regurgitation, mild tricuspid regurgitation, mild to
moderate mitral regurgitation, normal pulmonary artery pressure with pulmonic regurgitation.
Compared with previous study done 6/13/2015: there is improvement in the wall motion
and the present EF of 48% from 39%.
Chest AP: Cardiomegaly, minimal left pleural effusion, subsegmental atelectasis, right mid
lung field, Atherosclerotic aorta, thoracic spondylosis with dextroscoliosis and vascular
catheter in place
ADMITTING IMPRESSION
Calciphylaxis bilateral thigh
CKD Stage V secondary to DM Nephropathy and HPN Nephrosclerosis
HCVD
Type 2 DM
PERIOPERATIVE COURSE
Attached to standard ASA monitors
Inducted via GETA
BP: 150/100
4:00 PM PR: 60-65
O2 sat: 100%
IVF: D5 0.3% NaCL @ 20 gtts/min
Preoxygenation at 8LPM
Pre-induction with Midazolam 1mg and Fentanyl 75mcg.
Induction with Propofol in increments of 10mg
Neuromuscular blocker with Cisatracurium 10mg
DL using MAC 4 Blade and an ETT size 7.0 was cuffed and secured at level 20.
Maintenance with Sevoflurane
Operation started
Operation ended
Extubated
1:23AM
TIME OF DEATH
FINAL DIAGNOSES
Cardiopulmonary arrest secondary to shock multifactorial:
Hypovolemic shock
Septic shock secondary to Necrotizing Fascitis and Bacteremia
Such apparent shock results from at least 25%-30% loss of blood volume.
Advanced Trauma Life Support Classification of Hemorrhagic Shock
Class I Class II Class III Class IV
Blood loss (mL) < =750 750-1500 1500-2000 >=2000
Blood loss (% blood <=15 15-30 30-40 >=40
volume
Pulse rate (per <100 >100 >120 >=140
minute)
BP NORMAL NORMAL DECREASED DECREASED
Pulse pressure Normal or increased Decreased Decreased Decreased
Acidosis is the best indicator in early shock of ongoing oxygen imbalance at the tissue level.
Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L. 1., Jameson, J. L., & Loscalzo, J. (2015). Harrison's principles of internal medicine (19th edition.)
HYPOVOLEMIC SHOCK:
MEDICAL CARE
Primary treatment is to control the source of bleeding as soon as possible and to replace fluid.
Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L. 1., Jameson, J. L., & Loscalzo, J. (2015). Harrison's principles of internal medicine (19th edition.)
Barash, Paul G., Bruce F. Cullen, and Robert K. Stoelting. 2017. Clinical anesthesia (8th edition)
HYPOVOLEMIC SHOCK:
MEDICAL CARE
PRBCs should be transfused if the patient remains unstable after 2000 mL of crystalloid
resuscitation.
FFP generally is infused when the patient shows signs of coagulopathy, usually after 6-8 U of
PRBCs.
Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L. 1., Jameson, J. L., & Loscalzo, J. (2015). Harrison's principles of internal medicine (19th edition.)
Barash, Paul G., Bruce F. Cullen, and Robert K. Stoelting. 2017. Clinical anesthesia (8th edition)
HYPOVOLEMIC SHOCK:
MEDICAL CARE
Complications
Acidosis – Hypoperfusion, massive transfusion
Hypothermia
Cold fluids and blood products, opening of body cavities, decreased heat production, and
impaired thermoregulatory control
Coagulopathy
Dilution of clotting factors, consumption of clotting factors, and hyperfibrinolysis
blood products are stored in anticoagulation solutions
Electrolyte abnormalities
TRALI - Leukocyte antibodies transfused in plasma
Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L. 1., Jameson, J. L., & Loscalzo, J. (2015). Harrison's principles of internal medicine (19th edition.)
Barash, Paul G., Bruce F. Cullen, and Robert K. Stoelting. 2017. Clinical anesthesia (8th edition)
MASSIVE TRANSFUSION
PROTOCOL FOR
HEMORRHAGIC SHOCK
Despite significant advances in trauma management, mortality from hemorrhagic shock
remains the number one cause of death.
Data suggests that reconstituting components of blood to resemble whole blood have better
survival profile.
The variability in defining massive bleeding may result in variability initiating a MTP