CASE HISTORY:

Mr. XYZ, a 22-year-old gentleman, was on maintenance hemodialysis due to CKD. He was planned for a live related renal transplant on 31/8/2023. He was also a known hypertensive on regular medications, which were optimized recently. During routine dialysis on 28/8/2023, his BP was found to be 210/90mmHg, for which he was given sublingual nifedipine. Subsequently he developed headache along with drowsiness and slurred speech. His blood pressure was around 220/100mmHg in spite of the anti-hypertensive medications. He was shifted to the ER and labetalol infusion was started. CT brain was done, in view of his decreased responsiveness, which showed acute hemorrhage with surrounding edema in the right gangliocapsular and frontal regions with intraventricular extension in bilateral lateral and third ventricles with mass effacement and mild midline shift to left.

He was immediately admitted in the neuro ICU and opinion from neurologist was obtained. Repeat CT on the next day, did not show any interval changes. However, on 30^th August 2023, he became less responsive again, and repeat CT brain showed mild increase in the surrounding hypodensities (edema) with midline shift to left.

He was taken up for emergency decompressive craniectomy, after consulting the Neurosurgeon. The patient was also initiated on Continuous renal replacement therapy (CRRT), initially with no heparin anticoagulation and later on regional citrate anticoagulation. The serum sodium levels were monitored and maintained at 150mEQ/l through dialysis. His neurological status improved gradually. He was tracheostomised in view of prolonged ventilatory requirement. His limb power on the left side improved significantly and is now 4/5 in the left upper and lower limbs. The patient is now communicating well and is hemodynamically stable.

INTRA-DIALYTIC HYPERTENSION:

Intra-dialytic hypertension is defined as the increase in blood pressure from pre to post dialysis, which is an independent mortality risk predictor in dialysis patients. The mechanisms are not known completely, but are associated with chronic volume overload, activation of renin- angiotensin aldosterone axis and sympathetic system. It is also attributed to endothelial cell dysfunction, erythropoietin supplementation and bone mineral disease.

BLEEDING IN RENAL DISEASE PATIENTS:

Compared with the general population, patients with ESRD have a 10-fold greater risk of cerebral hemorrhage, 10-20 fold higher risk of subdural hematomas and a 100 fold risk of gastrointestinal bleeding. Hemorrhagic pericarditis, though very rare is also seen in patients on dialysis.

CAUSES INCLUDE:

1. Thrombocytopenia and platelet functional defects, impaired platelet aggregation and adhesion, complicated by uremia.
2. PTH (parathyroid hormone), which impairs platelet aggregation.
3. Increased nitric oxide synthesis, which prevents platelet aggregation and inhibiting vasoconstriction
4. Persistent anemia
5. Exposure of blood to the dialyser membrane, circuit tubing and microbubbles in circuit, leads to the activation of platelets and inflammatory cells
6. Administration of anticoagulants to avoid circuit clotting during HD, especially heparin by promoting platelet aggregation.

THE TAKE HOME POINTS:

The stringent monitoring of vitals for patients during hemodialysis has been the key point in diagnosing the intracranial hemorrhage, early and also performing CRRT to maintain the hemodynamics, while not allowing the intra-cranial hemorrhage from progressing, were crucial factors, which helped the patient recover significantly. This hypertensive emergency, though rare, has to be anticipated and managed appropriately to reduce the mortality and morbidity in patients on dialysis.

Dr. R. Balasubramaniyam
Chief Nephrologist
Kauvery Hospital Chennai

Dr. Rashmi Shivram
Resident – Nephrology
Kauvery Hospital Chennai