70year male with multiple organ dysfunction

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Unit 1

Interns

Dr. Sravya Kandala

Dr. Navya

Dr. Raheem

Dr. Gnanadha

Dr. Chetana

Dr. Ashfaq

Dr. Charan PGY1

Dr. Chandana PGY1

Dr. Sushmitha PGY2

Dr. Adithya PGY3

Dr. Praneeth PGY3

Dr. Praveen Naik Ass. Prof.

Dr. RAKESH BISWAS HOD

Here is a case I've seen:

Admission under Unit 1 on 01/03/2021

75year old male shepherd by occupation apparently alright 3months ago ,non diabetic,non hypertensive,chronic smoker( since 40years,2chuttas/day),chronic alcoholic (since 40years 90ml/day)

Was brought to casualty on 1/2/2021 night with ET tube insitu on portable mechanical ventilator

On asking the attendors they give the history of

generalized edema 3months back (now subsided) pain abdomen(Rt sided) since 3days,anuria since 3days and constipation since 1day and was intubated outside in view of falling sats(spo2 40%)

On Reviewing outside hospital notes it was written as pt was brought in gasping state, unconscious state .Bp :NR,PR:40bpm and was intubated on 28/2/2021 in view of falling sats and was having MODS,AKI(outside last known  creat on the day of intubation 3.6,urea 51) with severe life threatening metabolic acidosis(post intubation on SIMV on 28/2/2021 with Fio2 60% Ph 6.86,pco2 14.7,Hco3- 2.1,po2 342),on 1/3/2021 outside abg ph 7.35,pco2 26.8, hco3 14.7)outside ECG showed severe bradycardia (42bpm,regular)with junctional rhythm(absent p waves) ,low voltage complexes on chest leads(? secondary to COPD)

could be acute heart failure, myocardial depression secondary to severe metabolic acidosis

Outside CBP showed neurophilic leukocytosis(TLC 14,800,88% neutrophils) indicating some focus of sepsis

was treated outside with Iv antibiotics? unknown,iv fluids,iv steroids 

outside ECG

severe bradycardia (42bpm,regular)with junctional rhythm(absent p waves) ,low voltage complexes on chest leads(? secondary to COPD)

outside chest x ray

DAy 1(1/3/2021)

When pt was brought to casualty 

Pt is with ET tube insitu and on Ambu, conscious,moving all 4limbs

E4VTM6

Sats 99%

Bp 160/90

Grbs 115

PR 136bpm

JVP raised

his vitals were stable,no features of hypovolemia as written outside (resolved) 

Foleys catheterization was done outside

Pt was connected to mechanical ventilator CPAP VC mode as abg showed Po2 retension (Ph7.1,pco2 50,hco3 16.0)

Ecg 

chest x ray:AP view

With the history of Pain abdomen (right side),and constipation and sluggishness of bowel sounds differentials were made as

 1.? intestinal obstruction followed by perforation and hypovolemic shock 

2. ?acute appendicitis 

3. ?uremic ileus

Usg abdomen:collapsed  and aperistaltic bowel loops

  

DAY 2 (2/3/2021)

pt was slowly weaned off mechanical ventilation by 2/3/2021 afternoon

I/O 1500/1200

CUFF LEAK test

Before cuff leak

After cuff leak

The cuff-leak test has been proposed as a simple method to predict the occurrence of post-extubation stridor. The test is performed by cuff deflation and measuring the expired tidal volume a few breaths later (VT). The leak is calculated as the difference between VT with and without a deflated cuff. However, because the cuff remains deflated throughout the respiratory cycle a volume of gas may also leak during inspiration and therefore this method (conventional) measures the total leak consisting of an inspiratory and expiratory component.

This test consists of deflating the balloon cuff of the endotracheal tube to assess the air leak around the tube during expiration by measuring the expiratory tidal volume with and without a deflated cuff . A relatively large difference between these two values indicates that the cross-sectional area of the tracheal and/or upper airways is large enough to render the occurrence of post-extubation stridor, and therefore the possibility of re-intubation due to airway obstruction, unlikely

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065107/#:~:text=The%20cuff%2Dleak%20test%20has,and%20without%20a%20deflated%20cuff.

post extubation Abg

After extubation pt was taken for chest x ray PA view

x ray erect abdomen

no features s/o intestinal obstruction

reports on day 1 and day2

Aditya Sir Pg 3rd Yr: Everything is fitting in with Uremia causing ileus and pain abdomen.

Aditya Sir PGy3: Metabolic acidosis from AKI in the background of severe COPD explains his intubation.

The key here is what led to the AKI ? The hepatitic pattern is likely from congestive hepatopathy

DAY 3

70yr old with Multiorgan dysfunction syndrome

Acute kidney injury(maintenance phase ,urine output 800ml) secondary to ?Sepsis(Outside report of neutrophilic leukocytosis)

Worsesningg inspite of iv fluids and foleys indicating Renal AKI ,ruling out pre renal and post renal AKI

?Congestive hepatopathy secondary to acute heart failure which is secondary to severe high anion gap metabolic acidosis(resolved)

Chronic obstructive pulmonary disease

S-pain abdomen resolved, cough+, generalized weakness

O-Bp 130/70

PR 90

Cvs s1s2+

RS Abdominal breathing,reduced almost absent chest expansion obsereved

Barrel shaped chest

Harrisons sulcus

Accessory muscle hypertrophy at supraclavicular fossa

Pursued lip breathing

Pink puffer

?Nicotine stains on lips

CVS :Jvp not raised as seen at the time of admission

S1s2+,no murmurs

A-serial LFT's

Serial LFTs show decreasing AST,increasing ALT

Discussion on serial LFTs:Congestive hepatopathy

[3/4, 5:10 PM] Aditya Sir Genmed Pg 3rd Yr: Super. So at baseline the AST was higher than the ALT. ALP is normal and the bilirubin is only mildly elevated. 

This suggests that it is a purely hepatitic pattern and not a cholestatic pattern. 

Causes of Hepatitis can be broadly split into ITVHO - Infections, Toxins, Vascular, Hereditary and Other causes. 

Infections are most often viral - Hepatitis A to E and EBV, CMV, HSV and VZV. The produce a very characteristic elevation of enzymes to usually 1500 to 2000 and with ALT > AST. The half life of ALT is 3 to 4 weeks while that of AST is about 1 to 2 weeks. So it's unlikely to be an infection causing thia

[3/4, 5:12 PM] Aditya Sir Genmed Pg 3rd Yr: Toxins - The most common cause of toxin is Alcohol. Other toxins include Drugs, particularly Phenytoin, Valproate, Paracetamol, Isoniazid, Pyrazinamide and so on. He hasn't taken any of these has he ?

Classically, the pattern with toxin mediated hepatitis is ALT>AST, except with alcohol, which shows AST>ALT. 

Other unusual toxins are recreational drugs like Cocaine and Meth and also recreational mushrooms.

[3/4, 5:17 PM] Aditya Sir Genmed Pg 3rd Yr: Vascular - Ischemic Hepatitis, Congestive Hepatopathy and Acute Budd Chiari. Ischemic hepatitis is a forward flow failure and involves zone 1 to 3 of the Rappaport zones in the hepatic lobules of the liver. If zone 1 is involved, they could have a clinically significant feature - Hypoglycemia and Lactic Acidosis (hence why these are classically seen in Malaria) both of which appear to be absent in this patient. Also Ischemic Hepatitis is one of the only cause where the enzymes may rise as high as 5000s. Also, they should have a history of HFrREF, neither of which the patient has. 

Congestive Hepatopathy - Due to increased right sided heart pressures causing liver congestion. The enzymes in such a situation increase from anywhere between 20 to 30 fold of normal but almost always less than 1000. 

Acute Budd Chiari is also very similar to congestive hepatopathy in terms of biochemical picture. 

Importantly, all vascular causes show AST > ALT.

[3/4, 5:18 PM] Aditya Sir Genmed Pg 3rd Yr: Hereditary - Wilson's, Hereditary Hemochromatosis, Alpha 1 AT Deficiency. Flatly ruled out.

[3/4, 5:19 PM] Aditya Sir Genmed Pg 3rd Yr: Other causes - NASH, Autoimmune Hepatitis, Sickle Cell disease and quite common is Herbal Medicine use. Which can be considered a toxin too. Herbal medicine too produces a dramatic elevation of enzymes to levels of upto 2000 to 3000, on par with Viral Hepatitis.

[3/4, 5:19 PM] Aditya Sir Genmed Pg 3rd Yr: @⁨Dr.Chandana Vishwanatham⁩ What is your provisional diagnosis now ?

[3/4, 6:08 PM] Dr.Chandana Vishwanatham: Congestive hepatopathy?

[3/4,6:010PM]Aditya sir:Seems so to me too

Worsesning AKI with urea 220,Creat 8.3, Electolytes within normal limits

P -pt attendors were counselled about need for dialysis but they denied,did not give consent and want to continue on conservative management

2d Echo was done

Serum LDH 959 Iu/L(?DIC)

Discussion on DIC

[3/6, 11:14 AM] Aditya Sir Genmed Pg 3rd Yr: DIC 👍

[3/6, 11:15 AM] Dr.Chandana Vishwanatham: leptospira?focus of sepsis?

[3/6, 11:16 AM] Sai Charan Gen Med Pg KIMS: post antibiotics..!!

[3/6, 11:21 AM] Aditya Sir Genmed Pg 3rd Yr: Could suspect Strep Pneumo in a COPD guy. Or even Staph Aureus.

[3/6, 11:22 AM] Aditya Sir Genmed Pg 3rd Yr: We're not sure which antibiotic he received outside but it's catergorically unlikely he recieved a macrolide. A penicillin like Pip or Mero most likely which targets Strep and Staph well

[3/6, 5:46 PM] Aditya Sir Genmed Pg 3rd Yr: However now, I think congestive hepatomegaly maybe unlikely and I think the liver too had microvascular damage (just like the kidney) and suffered as a consequence of DIC. 

The most common cause of DIC is Sepsis and I think Sepsis explains everything in this patient.

[3/6, 5:47 PM] Aditya Sir Genmed Pg 3rd Yr: If you notice his outside medical records, you'll see that his BP was not recordable but his Pulse was palpable and had a rate of 40 BPM. This is very characteristic of a high output state, where you have shock but a pulse is palpable.

[3/6, 5:48 PM] Aditya Sir Genmed Pg 3rd Yr: So Hypovolemic, Obstructive and Cardiogenic shock are unlikely. It's most likely a distributive shock and the most common cause of a distributive shock is Septic Shock. 

The mortality rate from Septic shock in such elderly populace is very high and it's a miracle this man survived.

[3/6, 5:51 PM] Aditya Sir Genmed Pg 3rd Yr: It likely means that the causative agent of this septic shock was a community acquired infection. 

This could either be a common pathogen taking advantage of his lung compromise and elderly age (these are generally susceptible to usual antibiotics)

Or

It could a strong, drug resistant pathogen which marauded his body and caused severe end organ damage. (Usually result in death and are MDR)

So, I think we reached a fairly satisfactory conclusion to what his problem was. It's DIC secondary to Sepsis. But what caused the sepsis, I don't know.

[3/6, 5:51 PM] Aditya Sir Genmed Pg 3rd Yr: The key lies in which antibiotics he received ?

[3/6, 5:51 PM] Aditya Sir Genmed Pg 3rd Yr: He also did not receive any antibiotics in our hospital. Very uncanny.

[3/6, 5:53 PM] Aditya Sir Genmed Pg 3rd Yr: Btw DIC in kidney causes, what we commonly know as ATN due to microvascular dysfunction

[3/6, 5:55 PM] Dr.Chandana Vishwanatham: How can we confirm its DIC sir? thrombocytopenia and raised LDH enough?or should we send for PT aPTT

[3/6, 5:56 PM] Aditya Sir Genmed Pg 3rd Yr: You can.

[3/6, 5:56 PM] Aditya Sir Genmed Pg 3rd Yr: The hallmark of DIC is - "There is no single confirmatory test for DIC".

Could also be Ischemic Hepatitis because of shock

Diagnosis

70yr old with Multiorgan dysfunction syndrome and ?DIC secondary to ?sepsis

Acute kidney injury-Renal(maintenance) secondary to ?Sepsis(Outside report of neutrophilic leukocytosis)

?Congestive hepatopathy secondary to acute heart failure which is secondary to severe high anion gap metabolic acidosis(resolved) or ? Ischemic hepatitis secondary to shock

Chronic obstructive pulmonary disease