Dengue Fever-Induced Hypokalemic Paralysis in a Pregnant Patient: An Uncommon Presentation of a Common Disease

 Dengue fever is a globally prevalent, viral disease transmitted by Aedes mosquitoes, which is becoming increasingly common and can cause a range of symptoms, including fever, flu-like symptoms, and circulatory failure. Although it is classified as a non-neurotropic virus, research has suggested that dengue fever can also affect the nervous system and lead to conditions such as myositis, Guillain-Barré syndrome, or hypokalemic paralysis. We describe a case study of a young pregnant female with dengue-associated hypokalemic paralysis, who made a full recovery within 48 hours of receiving potassium supplementation. The case underscores the importance of recognizing and treating neurological complications of dengue fever promptly, particularly in areas where the disease is prevalent.

Dengue fever is a viral disease that is spread by Aedes mosquitoes, primarily in tropical and subtropical regions worldwide. It is becoming increasingly common, with 50 to 100 million infections recorded annually by the World Health Organization (WHO). In the year 2021, Pakistan has reported 48,906 cases and 183 deaths due to dengue fever [1]. Dengue fever can affect individuals of any age and can be life-threatening if it develops into severe dengue. Symptoms may include fever, flu-like symptoms, eye pain, dengue hemorrhagic fever, circulatory failure-induced shock, a decrease in platelet count (thrombocytopenia), and low concentration of red blood cells (anemia) [2]. Although classified as a non-neurotropic virus, various studies suggest that dengue may affect the nervous system. Acute neuromuscular weakness is thought to be due to myositis, Guillain-Barré syndrome, or hypokalemic paralysis during dengue. While numerous authors have reported hypokalemic paralysis associated with dengue, most studies are based on case reports [3-6]. We present an intriguing case of hypokalemic paralysis associated with dengue in a young, pregnant female who fully recovered within 48 hours of potassium supplementation.

A 30-year-old 26-week pregnant female patient presented to the emergency department with complaints of sudden onset of bilateral lower limb weakness, with the inability to walk for about eight hours prior to presentation. This was associated with high-grade fever (103°F), headache, nausea, vomiting, generalized body aches, and joint and muscle pains for three days. On examination, the patient was conscious, and oriented in time, place, and person. The patient's blood pressure was 100/65 mmHg, pulse rate was 108/minute, and oxygen saturation was 96% on room air. The patient was pale, mildly dehydrated, and anxious. On neurological examination, the patient was conscious, and oriented in time, place, and person. There was a decreased power of 3/5 in both lower limbs and a decreased tone. Deep tendon reflexes were absent in both lower limbs. Planter reflexes were normal. There were no signs of a sensory, cranial nerve, or autonomic dysfunction. While on upper limb examination, tone and reflexes were normal with a power of 5/5. The rest of the physical exam was without any relevant findings.

Laboratory investigations revealed a white blood cell count of 2700/μL, and platelet count was decreased (88,000/µl). Serum electrolytes showed decreased potassium of 2.5 mmol/L with normal sodium and chloride levels. The rest of the lab findings are mentioned in Table 1. The patient's thyroid profile and random blood glucose level were normal. The patient's dengue NS1 antigen was positive by the immunochromatographic method and the malarial parasite was negative on the rapid immunochromatographic assay. Typhus and leptospirosis were excluded by negative serology. The patient's urinalysis was unremarkable. The patient's nerve conduction study showed normal condition velocity and amplitude of nerve action potential. Based on the patient's history, clinical examination, and laboratory investigations, a diagnosis of dengue fever-associated hypokalemic paralysis was made. The patient was treated with potassium chloride at a rate of 10 mEq/hour in normal saline infusion, which resulted in clinical improvement of lower limb weakness. The patient was also started on oral potassium chloride tablets. On a subsequent day, the patient's electrolytes were normal. Fetal well-being was assessed using ultrasonography (Figure 1), which was normal. The patient was monitored for any electrolyte imbalance and any bleeding for 24 hours and was discharged home in stable condition with no muscle weakness and with normal electrolytes and renal function test.

	1st day of admission	2nd the day of admission	Normal value
White blood cells	2700/µL	3200/µL	4-11/µL
Hemoglobin	10.2 g/dl	10.2 g/dl	11.5-17.5 g/dl
Platelets	88,000/µL	92,000/µL	150-450/µL
Serum sodium	139 mmol/L	143 mmol/L	135-150 mmol/L
Serum potassium	2.57 mmol/L	3.6 mmol/L	3.5-5.1 mmol/L
Blood urea	8.6 mg/dl	14 mg/dl	10-50 mg/dl
Serum creatinine	0.56 mg/dl	0.6 mg/dl	0.42-1.06 mg/dl
Alanine transaminase	162 IU/L	160 IU/L	10-50 IU/L
Creatinine kinase	434 IU/L	370 IU/L	26-140 IU/L

Neurological symptoms associated with dengue fever include encephalitis, encephalopathy, aseptic meningitis, mononeuropathies, polyneuropathies, Guillain-Barré syndrome, myelitis, intracranial hemorrhage, and thrombosis. The development of these symptoms can be attributed to multiple factors, including the neurotropic effect of the dengue virus, the systemic effect of dengue infection, and injury caused by the immune system [7]. Hypokalemia resulting from dengue infection can lead to acute pure motor quadriparesis, but proper potassium correction can result in full recovery.

Our case report involves a pregnant female patient with bilateral lower limb weakness diagnosed with dengue-induced hypokalemic paralysis. When diagnosing hypokalemic paralysis, it is essential to consider Guillain-Barré syndrome as the most important differential diagnosis. Patients with dengue-associated Guillain-Barré syndrome may require intravenous immunoglobulins treatment, whereas those with dengue-associated hypokalemic paralysis typically show improvement soon after potassium is administered. Both conditions present with areflexic quadriparesis, although some asymmetry in reflexes may be observed along with preserved sensations and a flexor plantar response [8]. Normal nerve conduction studies, electromyography, and mildly raised serum creatine phosphokinase excluded Guillain-Barré syndrome and myositis in our patient, which can present similarly.

In a retrospective analysis of 29 hypokalemic paralysis patients, Garg et al. found that four patients had a history of fever and myalgia and were diagnosed with dengue fever, and they fully recovered with potassium supplementation [9]. In another cross-sectional study conducted in a tertiary care hospital in western India, among 5821 patients diagnosed with dengue, 154 (2.64%) had neurological manifestations, with the most common being encephalopathy, encephalitis, and syncope. Hypokalemic paralysis developed in 1.3% of the patients. This study is the largest reported study of neurological complications due to dengue (Figure 2) [10].

Our case report also highlights the effect of dengue fever on fetal well-being. The potential relationship between dengue fever and fetal congenital malformation is not well established. Sharma et al. reported an increased incidence of neural tube defects (NTDs) in newborns born during the dengue epidemic in a northern district of India, suggesting that the cluster of NTDs is likely due to dengue virus infection [11]. Our patient was 26 weeks pregnant at the time of presentation with good fetal movements. Fetal well-being was assessed using ultrasonography and cardiotocography, which were normal.

Hypokalemic paralysis is a rare complication of dengue fever and other infectious diseases, such as leptospirosis and chikungunya [12]. The exact mechanism of hypokalemia in dengue fever remains unclear, but Jha and Ansari proposed two possible mechanisms for this phenomenon: redistribution of potassium in cells or transient renal tubular abnormality leading to increased urinary potassium excretion. This instance emphasizes the link between hypokalemic paralysis and dengue fever [3]. Medical practitioners need to be familiar with this relationship, particularly in regions such as Pakistan, where atypical signs of dengue fever are increasingly prevalent. This awareness can aid in the timely diagnosis and management of the illness.

Indeed, this case report highlights the need for healthcare providers to be vigilant for potential neurological complications in patients with dengue fever, especially in regions where dengue is endemic. Additionally, this case emphasizes the importance of prompt diagnosis and treatment of hypokalemic paralysis in patients with dengue fever, as potassium supplementation can lead to a rapid and complete recovery. Finally, this case report underscores the importance of monitoring fetal well-being in pregnant patients with dengue fever, as this infection can potentially cause harm to the fetus. Overall, this case report provides valuable insights into the potential complications and management of dengue fever, particularly in pregnant patients.

References

1. World Health Organization. Dengue guidelines for diagnosis, treatment, prevention, and control: new edition. (2009). https://apps.who.int/iris/handle/10665/44188.
2. Hasan S, Jamdar SF, Alalowi M, Al Ageel Al Beaiji SM: Dengue virus: a global human threat: a review of the literature. J Int Soc Prev Community Dent. 2016, 6:1-6. 10.4103/2231-0762.175416
3. Jha S, Ansari MK: Dengue infection causing acute hypokalemic quadriparesis. Neurol India. 2010, 58:592-4. 10.4103/0028-3886.68657
4. Roy A, Tripathi AK, Verma SP, Reddy H, Jain N: Acute hypokalaemic quadriparesis in dengue fever. BMJ Case Rep. 2011, 2011:10.1136/bcr.11.2010.3514
5. Gupta DK, Vaish AK, Arya RK, Chaudhary SC: Hypokalaemic quadriparesis: an unusual manifestation of dengue fever. BMJ Case Rep. 2011, 2011:10.1136/bcr.12.2010.3673
6. Jain RS, Handa R, Prakash S, Nagpal K, Gupta P: Acute hypokalemic quadriparesis: an atypical neurological manifestation of dengue virus. J Neurovirol. 2014, 20:103-4. 10.1007/s13365-014-0232-z
7. Chauhan L, Matthews E, Piquet AL, et al.: Nervous system manifestations of arboviral infections. Curr Trop Med Rep. 2022, 9:107-18. 10.1007/s40475-022-00262-9
8. Verma R, Sharma P, Garg RK, Atam V, Singh MK, Mehrotra HS: Neurological complications of dengue fever: experience from a tertiary center of north India. Ann Indian Acad Neurol. 2011, 14:272-8. 10.4103/0972-2327.91946
9. Garg RK, Malhotra HS, Verma R, Sharma P, Singh MK: Etiological spectrum of hypokalemic paralysis: a retrospective analysis of 29 patients. Ann Indian Acad Neurol. 2013, 16:365-70. 10.4103/0972-2327.116934
10. Kulkarni R, Pujari S, Gupta D: Neurological manifestations of dengue fever. Ann Indian Acad Neurol. 2021, 24:693-702. 10.4103/aian.AIAN_157_21
11. Sharma JB, Gulati N: Potential relationship between dengue fever and neural tube defects in a northern district of India. Int J Gynaecol Obstet. 1992, 39:291-5. 10.1016/0020-7292(92)90260-P
12. Gutch M, Agarwal A, Amar A: Hypokalemic quadriparesis: an unusual manifestation of dengue fever. J Nat Sci Biol Med. 2012, 3:81-3. 10.4103/0976-9668.95976

Why Do We Find It So Hard To Resist Treats Like Chocolate Bars? Scientists Discover Sweets Change Our Brain.

 

Regular consumption of high-fat and high-sugar foods rewires the brain to subconsciously prefer these unhealthy options due to changes in the brain’s dopaminergic system responsible for motivation and reward.

Why is it so hard to resist chocolate bars, chips, and fries while shopping at the supermarket? According to researchers at the Max Planck Institute for Metabolism Research in Cologne and Yale University, consuming foods high in fat and sugar can actually alter our brains. Regular consumption, even in small amounts, trains the brain to crave these foods in the future.

Why do we like unhealthy and fattening foods so much? How does this preference develop in the brain? “Our tendency to eat high-fat and high-sugar foods, the so-called Western diet, could be innate or develop as a result of being overweight. But we think that the brain learns this preference,” explains Sharmili Edwin Thanarajah, lead author of the study.

To test this hypothesis, the researchers gave one group of volunteers a small pudding containing a lot of fat and sugar per day for eight weeks in addition to their normal diet. The other group received a pudding that contained the same number of calories but less fat. The volunteer’s brain activity was measured before and during the eight weeks.

Our brain unconsciously learns to prefer high-fat snacks

The brain’s response to high-fat and high-sugar foods was greatly increased in the group that ate the high-sugar and high-fat pudding after eight weeks. This particularly activated the dopaminergic system, the region in the brain responsible for motivation and reward. “Our measurements of brain activity showed that the brain rewires itself through the consumption of chips and co. It subconsciously learns to prefer rewarding food. Through these changes in the brain, we will unconsciously always prefer the foods that contain a lot of fat and sugar,” explains Marc Tittgemeyer, who led the study.

During the study period, the test persons did not gain more weight than the test persons in the control group and their blood values, such as blood sugar or cholesterol, did not change either. However, the researchers assume that the preference for sugary foods will continue after the end of the study. “New connections are made in the brain, and they don’t dissolve so quickly. After all, the whole point of learning is that once you learn something, you don’t forget it so quickly,” explains Marc Tittgemeyer.

Reference: “Habitual daily intake of a sweet and fatty snack modulates reward processing in humans” by Sharmili Edwin Thanarajah, Alexandra G. DiFeliceantonio, Kerstin Albus, Bojana Kuzmanovic, Lionel Rigoux, Sandra Iglesias, Ruth Hanßen, Marc Schlamann, Oliver A. Cornely, Jens C. Brüning, Marc Tittgemeyer, and Dana M. Small, 22 March 2023, Cell Metabolism.

Why More People are Getting Allergies and Why They’re Getting Worse.

Allergies have intensified over the last few decades. An estimated 30 to 40 percent of the global population has some form of allergy, and experts say that number could rise to 50 percent by the year 2030. So what’s behind this? Research shows it’s a complicated picture, with climate change, our stress levels, and genetics all playing roles. We talk to medical anthropologist Theresa McPhail, author of the new book “Allergic,” about what the latest research shows on diagnostics, treatment, and what we can do to cope with our allergies in a “changing world.”

Guests:

Theresa MacPhail, medical anthropologist and associate professor of Science and Technology Studies, Stevens Institute of Technology; author, "Allergic: Our Irritated Bodies in a Changing World"

 

Is the human brain actually made up of 60% fat?

 

The human brain, often hailed as the most remarkable organ in the human body, continues to captivate both scientists and the general public alike. After all, it is an intricate network of neurons, glial cells, and supporting structures, each playing a vital role in the functioning of this remarkable organ. Hence, as advancements in neuroscience unfold, it is crucial to dispel misconceptions and clarify misconstrued information about this fascinating organ. In this part of the Know Your Body series, we address a commonly held belief: that the human brain is made up of 60 percent fat. But, is it true? “While it is true that the brain contains a significant amount of lipids (fats), the notion that it consists of 60 percent fat is an oversimplification and requires further clarification,” said Dr. S Ramesh, neurosurgeon, Kamineni Hospitals, Hyderabad. Docosahexaenoic acid is a structural constituent of membranes, specifically in the central nervous system. Its accumulation in the fetal brain takes place mainly during the last trimester of pregnancy and continues at very high rates for up to five-six years, said neurologist Dr. Sudhir Kumar.

Blood sugar maintenance mechanism revealed in DNA Study.

 

A large, worldwide DNA study has shed light on how healthy blood sugar levels are maintained after eating—and how that process may go wrong. The findings, published Thursday in Nature Genetics, may inform treatment for type 2 diabetes, which affects over 460 million people worldwide.

The hormone insulin helps regulate levels of blood sugar, or glucose. People with type 2 diabetes cannot regulate their glucose levels, either because they don’t secrete enough insulin when glucose levels increase, or because their cells are less sensitive to insulin, a condition called insulin resistance.

Risk factors contributing to type 2 diabetes include being overweight, older, obese, inactive, or genetically predisposed. If untreated, type 2 diabetes can lead to complications including eye disease, kidney disease, nerve damage, heart attack, and stroke risk.

Most insulin resistance studies have focused on the fasting state hours after a meal when insulin is acting on the liver. But some people spend more time in a fed state when insulin acts on muscle and fat tissues. Poorly understood molecular mechanisms underlying insulin resistance following a glucose challenge such as a sugary drink may play a key role in type 2 diabetes development.

In order to better understand these mechanisms, scientists used genetic data from 28 studies, encompassing more than 55,000 normal participants without type 2 diabetes, seeking genetic variants that influenced insulin levels two hours after a sugary drink.

The team identified 10 new loci—the physical locations of genes on chromosomes—associated with insulin resistance. Eight of these loci were also associated with a higher risk of type 2 diabetes. The gene that codes for GLUT4, a critical protein responsible for insulin-regulated glucose uptake into fat and muscle cells, is on one newly identified locus associated with a reduced amount of GLUT4 in muscle tissue.

Seeking additional genes that affect glucose regulation, the researchers investigated cell lines from mice. They discovered 14 genes that played a significant role in GLUT 4 transport and glucose uptake; nine had not previously been linked to insulin regulation.

Further experiments showed that these genes altered the ability of the GLUT4 protein to move from inside the cell to its surface. The less GLUT4 that makes its way to the cell surface, the poorer the cell’s ability to remove glucose from the blood. Given that problems regulating blood glucose after a meal can be an early sign of increased type 2 diabetes risk, the researchers hope their insights into the mechanisms involved will lead to better care for prediabetics.

“Our findings open up a potential new avenue for the development of treatments to stop the progression of type 2 diabetes,” Claudia Langenberg, director of Queen Mary University of London's Precision Healthcare University Research Institute, said in a statement. “It also shows how genetic studies of dynamic challenge tests can provide important insights that would otherwise remain hidden.”