51 year old male with AMS and acute kidney injury Overview
- Presenting Complaint
- Patient History
- Review of Systems
- Physical Examination
- Diagnostic Test
- Diagnostic Imaging
- Diagnosis and Management
- Discussion
A 51-year-old man presented to the Emergency Department with paresis in right side and altered consciousness.
- History of presenting
- Past Medical/Social history
- Past surgical history
- Family history
- Current Medication
At day 3 of hospitalization, he developed anuria, was tetraparetic and his creatinine value increased to 3.9 mg/dL. Another CT was performed that continued showing no acute ischemic insults. At this point, still believing in neurologic disease, the patient was submitted to lumbar puncture and magnetic resonance imaging, both without pathological findings
General
Heent
Neck
Cardiovascular
Lungs
Abdomen
Extremities
Skin
Neurological Exam
- Bio Chemistry
- Pathology
- Microbiology
- Hematology
- Miscellaneous
Sodium: WNL meq/L( normal 135-145 meq/L)
Potassium: WNL meq/L (normal 3.5-5.0 meq/L)
Chloride: WNL meq/L(normal 96-108 meq/L)
Bicarb: WNL meq/L(normal 22-30 meq/L)
Magnesium: WNL mg/dl ( normal 1.7 to 2.2 mg/dL )
Phos.: 5.8 mg/dl ( normal 2.8 to 4.5 mg/dL)
Bun: 180 mg/dl ( normal 6-23 mg/dL)
Creat: 4.5 mg/dl ( normal 0.7 -1.3 mg/dL)
Liver Enzymes - SGOT/AST: WNL U/L ( normal 1-35 )
SGPT/ ALT: WNL U/L ( normal 1-45 )
GGT: WNL U/L ( normal 8-38 )
Direct Bilirubin: WNL mg/dl ( normal 0.1-0.3 )
Total Bilirubin: WNL mg/dl ( normal 0.1 - 1.2 )
UA: A urine exam showed more than 1 million leucocytes, 60 000 red cells, hyaline and granulose cylinders, and a 944 mg/dL protein
miscellaneous : HIV, B and C hepatitis, VDRL Negative
blood, urine and tracheal cultures were all negatives.
Hemoglobin: WNL g/dl ( normal 13.9 -16.3)
Hematocrit: WNL % ( normal 42-52 % )
White Count: WNL ( normal 4,500 to 11,000 WBCs per microliter)
Platelets: WNL ( normal 150,000 to 450,000 platelets per microliter)
Differential: WNL
- CT Scan
- Xray
- MRI
- Ultrasound
- Echo
- Endoscopic
- Miscellaneous
normal
normal
normal
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1. what is the differntial diagnosis of this case ? ( atleast 4 recommended ) . give alteast 4 plausible choices with one right answer and explanation for each choice.
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There are few reported cases in the literature of star fruit toxicity [Table 2]. Notice that time since fruit ingestion and clinical presentation is highly variable, as so the amount ingested. From the published articles it can be concluded that if the patient has an empty stomach he does not need to consume a large amount of the fruit to develop the toxicity. On the other hand, a massive quantity (just like our case with 50 star fruits), independent of fasting, is a risk factor for neuro and nephrotoxicity.[2] We do not know, however, the precise maximum recommended amount of fruit or juice beyond which toxicity would be likely to appear.
Star fruit is a high source of oxalate. That explains the gastrointestinal symptoms that patients usually complain. They were not due to uremia as uremic symptom cannot develop soon after ingestion and suggest direct corrosive injury of oxalate in the digestive tract.[4]
The nephropathy induced by oxalate occurs a few hours later. The mechanism by which tubular damage occurred is the obstruction of renal tubules by these crystals as well as apoptosis of the renal tubular epithelial cells.[5]
The nephrotoxicity is strictly related to neurotoxicity. Star fruit has a neurotoxin called caramboxin, which has renal excretion and can pass through the blood-brain barrier. When renal function is abnormal there is an elevation of caramboxin in the central nervous system that results in neurological symptoms such as hiccups, paresis, seizure, coma and even death.[2,6] Moreover, there is no assay for caramboxin level yet available.
Neto et al.[7] had classified clinical symptoms of intoxication in uremic patients as 1) mild: hiccups (94%), vomiting (69%), and insomnia; 2) moderate: psychomotor agitation (66%), sudden-onset limb numbness, paresthesias (tingling/pricking) (41%), and muscle weakness; and 3) severe: moderate to severe mental confusion progressing to coma, seizures (22%) progressing to status epilepticus, and hemodynamic instability progressing to hypotension and shock.[7,8]
The treatment depends on clinical presentation, varying from conservative to dialysis. Some case reports used prednisolone in low doses,[9,10] urinary alkalization,[11] and diuretic therapy, all without a good evidence level.[12] Dialysis, on the contrary, seems the most reasonable treatment especially when neurological symptoms are present, since it is believed that caramboxin is dialyzable and may increase oxalate clearance, apart from the removal of uremic toxins.[2,10] However, there are no studies describing the use of hemodialysis for the sake of removal of oxalate per se without any other nephrological indications. We think that earlier dialysis can be performed if star fruit intoxication is hypothesized, especially with a disturbance in the conscious level or other neurological feature (peritoneal dialysis has been shown to be of no benefit, especially in these type of patients).[10,13,14] In our case, after initiation of dialysis sessions patients paresis improved. Dialysis could be started sooner even without classic indications due to severe neurological impairment, but star fruit intoxication was not one of our firsts differentials diagnosis.
Recently the effect of N-acetylcysteine on star fruit induced acute kidney injury was studied in animal models. The results suggest that this drug can reduce oxidative stress, oxaluria, and inflammation, attenuating renal dysfunction in the final analysis.[1] It is important to emphasize that acute events related to star fruit intoxication have a good prognosis. Every case reported in the literature had a recovery in renal function and no deaths. In chronic kidney disease, however, death can occur in 61% and 42% of patients with seizure and confusion, respectively.[2