Case Presentation
A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.
Vitals
HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)
ECG
He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.
In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.
ABG Findings
pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L
As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern.
He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters.
The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).
For the Inquisitive Minds
- The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
- His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
- Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
- Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
- What was the necessity for carrying out SLED for this patient?
- Why was this patient not immediately cardioverted in the ER?
- If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
- How differently would you have managed this patient?
1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
To ruleout the common causes we need to look for the following
1. RA RV dilation and D shapprd LV – if we expect PTE
2. Comat tails – pulmonary edema
3. Sea shore appearance and loss of sliding sign pneumothorax
4. Wall motion abnormality if in MI and poor Ejection fraction as he is in acidosis
5. Shrunken kidney
2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
Yes. EF will increase once the acidosis and potassium is corrected
3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
As he was hemodynamicaly unstable on presenting to ER, AV fistula may not be functioning good, but as the patient becomes stable, AVFistula will start functioning later
4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
Yes. As imminent cardiac arrest is anticipated, o2 by NRBM will be useful in denitrogenization and increase apnoea time. Which will be useful to prevent hypoxia during resuscitation
5. What was the necessity for carrying out SLED for this patient?
Regular Hemodialysis can’t be done in unstable patients
6. Why was this patient not immediately cardioverted in the ER?
Cardioversion would have been the right choice.
May be the author would have planed to wait and watch as the cause was easily reversible and the patient was intermittently getting stable vitals ( as evidenced by appearance of pulseoxymetry wave forms and saturation. )
7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
Calcium chloride or calcium gluconate, Sodium bicarbonate, dextrose insulin
8. How differently would you have managed this patient?
I would have cardioverted immediately and then proceed to antihyperkalemic measures including SLED
Dr V P Chandrasekaran
India
(My mentor and guide)
1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
To ruleout the common causes we need to look for the following
1. RA RV dilation and D shapprd LV – if we expect PTE
2. Comat tails – pulmonary edema
3. Sea shore appearance and loss of sliding sign pneumothorax
4. Wall motion abnormality if in MI and poor Ejection fraction as he is in acidosis
5. Shrunken kidney
2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
Yes. EF will increase once the acidosis and potassium is corrected
3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
As he was hemodynamicaly unstable on presenting to ER, AV fistula may not be functioning good, but as the patient becomes stable, AVFistula will start functioning later
4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
Yes. As imminent cardiac arrest is anticipated, o2 by NRBM will be useful in denitrogenization and increase apnoea time. Which will be useful to prevent hypoxia during resuscitation
5. What was the necessity for carrying out SLED for this patient?
Regular Hemodialysis can’t be done in unstable patients
6. Why was this patient not immediately cardioverted in the ER?
Cardioversion would have been the right choice.
May be the author would have planed to wait and watch as the cause was easily reversible and the patient was intermittently getting stable vitals ( as evidenced by appearance of pulseoxymetry wave forms and saturation. )
7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
Calcium chloride or calcium gluconate, Sodium bicarbonate, dextrose insulin
8. How differently would you have managed this patient?
I would have cardioverted immediately and then proceed to antihyperkalemic measures including SLED