The present study reports the case of an elderly male inpatient with uraemia who had a sudden onset of numbness and weakness in the right limbs during sleep at night, accompanied by blurred and double vision, during the induction of haemodialysis (HD). Cranial computed tomography and magnetic resonance imaging revealed signs of brainstem haemorrhage. Consequently, a proactive treatment approach was adopted for decreasing the blood and intracranial pressures of the patient, and regular HD was continued. The condition of the patient improved, and the limbs showed no impairment of sensation, with normal movement. To the best of our knowledge, this is the first reported case of an inpatient with uraemia undergoing HD who developed a sudden brainstem haemorrhage during the induction phase of HD and completely recovered after conservative treatment. This unusual case deserves the attention of all clinicians, who should pay more attention to the patients with spontaneous brainstem hemorrhage.
Chronic kidney disease (CKD) is a rapidly increasing global health burden and an important risk factor for cerebrovascular diseases (
The present study reports the case of an elderly male patient with uraemia who suffered from ICH at night in hospital, during the induction of haemodialysis (HD). On the basis of neurosurgery guidance, an active treatment approach was adopted for controlling the blood and intracranial pressures of the patient, and to continue regular HD. The condition of the patient improved, and the limbs showed no impairment of sensation, with normal movement lastly.
A 67-year-old Han Chinese male patient was admitted to Nephrology Department of Baoding First Central Hospital (Baoding, China) on 25th May 2022. The patient had been diagnosed with intermittent bilateral lower limb oedema 9 years before, and was experiencing chest tightness for the past 1 month. He was diagnosed with coronary atherosclerotic heart disease 4 years before, and with hypertension 2 years ago, with a maximum blood pressure (BP) of 190/100 mmHg; however, his BP was not monitored regularly. When he was diagnosed with bilateral lower extremity oedema 9 years before in our hospital, he had a urine protein level of 3+ (normal range, negative), 24-h urine protein level of 9.1 g (normal range, <150 mg), serum creatinine level of 89 µmol/l (normal range, 46.2-78.3), cholesterol level of 13.3 mmol/l (normal range, 3.2-5.2), triglyceride level of 2.40 mmol/l (normal range, 0.25-1.71), albumin level of 23.37 g/l (normal range, 40-55) and total protein level of 49.9 g/l (normal range, 60-85). The patient was diagnosed with nephrotic syndrome but refused to undergo renal biopsy. Methylprednisolone (40 mg once daily) and compounded cyclophosphamide (50 mg twice daily) were recommended. His condition improved following the above treatment and he was subsequently discharged. However, he was not followed up regularly as an outpatient. He was diagnosed with elevated creatinine levels 2 years ago and received oral herbal medications for around 1 year, but the specific name, dosage and frequency were unknown. Without regular re-evaluation of renal function. The patient developed chest tightness with weakness and shortness of breath 10 days prior to presentation to the hospital, which worsened after activity, and was admitted to our hospital for further treatment.
Physical examination at admission revealed the following findings: BP of 165/108 mmHg, anaemic appearance, heart rate of 105 beats/min, and facial and bilateral lower limb oedema. Ultrasonography showed that both kidneys were shrunken with diffuse lesions. The results of major laboratory tests conducted at the hospital are shown in
On 14th May 2022, the patient had a sudden onset of weakness and numbness in the right limb during sleep at night, which was accompanied by blurred and double vision, without consciousness or limb movement disorder, and his BP was 186/105 mmHg. Physical examination showed normal muscle strength of the upper right limb and grade IV muscle strength of the lower right limb. Bilateral pathological signs were absent. Urgent cranial computed tomography (CT) (
On 17th May, re-evaluation via cranial CT (
On 31st May, cranial magnetic resonance imaging and magnetic resonance angiography (
CKD and stroke are closely related, and the prevalence and mortality of stroke are higher among patients with CKD, particularly in those with uraemia (
SBH has the worst prognosis of all cerebral haemorrhages and lacks uniform diagnostic criteria (
The present elderly male patient, who had a 9-year history of nephrotic syndrome, a 4-year history of coronary artery disease and a 2-year history of hypertension, was admitted to the hospital with uraemia combined with heart failure, and was treated with conventional HD. During the initial phase of HD, the patient suddenly experienced SBH at night during sleep, with a significant increase in BP. SBH may have occurred due to traditional factors such as hypertension, heart failure and hyperlipidaemia, or to non-traditional factors such as proteinuria, uraemic toxins or anaemia. In addition, it may be associated with the pathological alterations in haemodynamics caused by HD. Sudden onset of SBH during night-time sleep is considered to be associated with a significant increase in nocturnal BP. Clinical guidelines recommend 24-h ambulatory BP monitoring in patients with CKD to detect nocturnal hypertension and to help clinicians to treat it with antihypertensive therapy (
The incidence of SBH is low, accounting for 5-10% of all ICH cases. SBH is characterised by acute onset, rapid deterioration and a high mortality rate (56-61.2%); hence, it is the worst type of haemorrhagic stroke. The mortality rate of SBH varies greatly due to differences in the bleeding site and quantity; however, the prognosis of the majority of patients remains markedly poor (
In the present case study, the patient was conscious during the onset of SBH, and CT revealed <5 ml cranial bleeding. Since the patient had uraemia, hypertension and coronary disease, surgery was relatively contraindicated, and conservative treatment was considered more suitable instead. Tranexamic acid may be safely and effectively administrated for acute spontaneous intracerebral hemorrhage (
Moreover, intravenous dehydrating agents are often used to correct plasma osmotic level and reduce intracranial pressure during the acute period in patients with intracerebral hemorrhage. Those dehydrating agents generally include albumin, dexamethasone, mannitol and glycerin fructose. Mannitol and glycerol fructose are the most commonly used in clinical practice. Intravenous infusion of mannitol has a rapid effect and a relatively short drug action time, but it is not suitable for patients with renal insufficiency. By contrast, glycerin fructose has a slower effect, but its drug action time is longer, which is particularly suitable for patients with renal insufficiency. Intravenous albumin or dexamethasone can also be applied to increase clinical efficacy apart from the ones mentioned above. In brief, the specific type and dosage of drugs should be selected according to the patient's condition, including the quantity and location of intracranial hemorrhage, and the patient's state of consciousness (
The present patient clinically manifested with hypoalbuminemia, hyperkalemia, hypocalcemia and hyperphosphatemia (
In conclusion, to the best of our knowledge, this is the first case that reported sudden onset of SBH in a patient with uraemia during the induction of HD. Although this patient still need to be improved on his treatment in acute stage of SBH, the present study may have clinical guidance for other patients similar to him. Conservative treatment is suitable for mild cases of SBH, but not severe ones. Since the onset of the SBH is sudden, and the therapeutic effects and prognosis are usually poor, prevention is especially important. It is of great clinical importance to actively screen the risk factors of SBH in patients with CKD, and to promptly control hypertension, hyperglycaemia and hyperlipidaemia. Hence, systematic evaluation of the aforementioned factors can help clinicians to select an appropriate treatment strategy and predict prognosis (
Not applicable.
The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
XL conceived and designed the study. YG acquired the data. RJ, XL and YG analyzed and interpreted the data and drafted the manuscript. XL and RJ confirm the authenticity of all the raw data. All authors critically revised the manuscript for important intellectual content. All authors read and approved the final manuscript.
The treatment of this patient was conducted in accordance with established clinical practice standards (
Written consent was obtained for the publication of the patient's data and images in the present case report.
The authors declare that they have no competing interests.
(A) Brain CT on 14th May 2022 showed patchy high density in the brainstem with clear borders, which was considered to be a haemorrhage. (B) Brain CT on 17th May showed patchy high density in the brainstem with clear borders, which was considered to be a haemorrhage slightly increased compared with that of 14th May. (C) Brain CT on 27th May showed patchy high density in the brainstem with clear borders, which indicated that the haemorrhage appeared to be decreasing in extent and had a reduced density compared with that of 17th May. The red arrow shows the haemorrhage site. CT, computed tomography.
Cranial magnetic resonance imaging + magnetic resonance angiography on 31st May showed a piece of (A) short T1 and (B) long T2 dominant mixed signal shadow in the cerebral bridge, surrounded by low signal. (C) fluid attenuated inversion recovery and (D) diffusion-weighted imaging showed high signal locally, and cerebral bridge haematoma was considered. (E and F) The lumen of the M1 segment of the left middle cerebral artery was slightly narrowed, and the posterior cerebral artery was stiffened bilaterally, with uneven lumen thickness and slightly reduced branches, which indicated cerebral arteriosclerosis. The red arrow shows the haemorrhage site.
Results of laboratory examination change in hospital.
Investigation | Normal range | Day 1 | Day 3 | Day 7 | Day 14 |
---|---|---|---|---|---|
Hb (g/l) | 110.0-150.0 | 63.5 | 68.3 | 78.4 | 85.9 |
Plt (x109/l) | 125.0-350.0 | 342.9 | 295.4 | 312.4 | 288.2 |
Alb (g/l) | 40.0-55.0 | 35.1 | 32.7 | 35.4 | 38.1 |
Urea (mmol/l) | 2.6-7.5 | 38.1 | 18.3 | 24.9 | 15.7 |
CREA (µmol/l) | 41.0-73.0 | 1,076.7 | 665.7 | 485.2 | 514.3 |
Serum sodium (mmol/l) | 137.0-145.0 | 134.7 | 139.6 | 142.3 | 139.6 |
Serum potassium (mmol/l) | 3.5-5.3 | 5.9 | 4.8 | 5.1 | 4.7 |
Serum calcium (mmol/l) | 2.1-2.5 | 1.8 | 1.9 | 2.0 | 2.1 |
Serum phosphorus (mmol/l) | 0.8-1.5 | 2.1 | 1.7 | 1.4 | 1.3 |
BNP (pg/ml) | 0.0-100.0 | 4,185.2 | 2,645.9 | 1,856.7 | 1,223.6 |
dimer (mg/l) | 0.0-0.5 | 2.1 | 1.6 | 1.2 | 0.9 |
CRP (mg/l) | 0.0-10.0 | 10.3 | 9.3 | 8.5 | 7.2 |
Fbg (g/l) | 1.8-3.5 | 4.6 | 4.2 | 3.9 | 3.4 |
LVEF (%) | 45.0-55.0 | 38.0 | 42.0 | 45.0 | 51.0 |
Hb, hemoglobin; Plt, platelet; Alb, albumin; CREA, creatinine; BNP, brain natriuretic peptide; Fbg, fibrinogen; CRP, C-reactive protein; LVEF, left ventricular ejection fraction.