Idiopathic Hyperhidrosis after Trauma: A Case Report

doi:10.21203/rs.3.rs-5279798/v1

Background

Hyperhidrosis is the secretion of excess sweat beyond what the body needs for homeostatic regulation. Secondary hyperhidrosis is usually related to an underlying cause, mostly a medical condition, or extrinsic factors such as drugs or trauma to the central nervous system. Treatment can be based on resolution of the underlying cause or symptomatic management.

Case presentation

A 53-year-old male collided with a motor-vehicle at 40 km/h. Lacerations on his forehead and multiple abrasions on his lower extremities were treated shortly; however, the patient soon started complaining of excessive sweating. Despite several imaging and laboratory tests for central and peripheral causes, we failed to identify the reason for excessive sweating. Symptomatic treatments such as anticholinergics and ganglion block also failed, and only after hemodialysis did the patient stay dry for a short time. Fortunately, his symptoms disappeared shortly after discharge.

Conclusion

The patient presented with great discomfort after trauma, with an undisclosed cause. Medical treatment and intervention failed to improve the symptoms; however, hemodialysis alone relieved the patient. Whether it was medically or traumatically induced, uncontrolled sweating was controlled by hemodialysis.

Hyperhidrosis

hemodialysis

trauma

chronic kidney disease

The body dissipates heat via radiation, conduction, convection, and evaporation, with sweating being the most important pathway. The rapid onset of sweating is crucial, as, even small increases in body temperature can reduce performance [1]. The human body contains approximately four million sweat glands, divided into eccrine and apocrine types, with the eccrine glands accounting for 90% of them. Eccrine glands are distributed across the entire body and play a play a key role in thermoregulation [2]. These glands are innervated by sympathetic cholinergic nerve fibers, and in addition to thermoregulation, they also respond to emotionally induced sweating via catecholamines [3, 4]. Apocrine sweat glands are found selectively in areas such as the axillary, anogenital, perimammary, periumbilical, preputial, scrotal, eyelid, and external auditory conduit regions [5]. However, according to Atkins et al., their role in hyperhidrosis, particularly in the axilla, is considered to be of minor importance [6].

Acetylcholine and noradrenaline are the two main neurotransmitters that regulate sweat secretion [2]. Innervation of the eccrine sweat glands is affected by the hypothalamus, which is the integration center for all thermosensory afferent fibers from the pons and medulla to the spinal cord [1]. The fibers then undergo synaptic switching, mostly in the paravertebral sympathetic ganglia. Subsequently, they release acetylcholine as a peripheral neurotransmitter that binds to the postsynaptic muscarinic receptors of the eccrine sweat glands and triggers sweating [7].

Hyperhidrosis is the secretion of excess sweat beyond what the body needs for homeostatic regulation. It is not merely an increase in the absolute amount of sweat but rather a change in the kinetics of sweat, that is, a change in the ability to control sweating, resulting in abnormally strong sweating, even upon small triggers [1].

Primary hyperhidrosis originates from the normal eccrine sweat glands that overexpress neurogenic activity. Compound dysfunction of the autonomic nervous system and deficiency in the central regulation of emotions are some of the major etiologies of primary hyperhidrosis [8]. Secondary hyperhidrosis typically has an underlying cause. Although most cases of secondary hyperhidrosis area generalized, focal cases also exist [9]. Common causes of hyperhidrosis include endocrine/metabolic disorders (diabetes mellitus, hyperthyroidism, and hyperaldosteronism), acute fever (bacteremia and tuberculosis), malignancies (carcinoid, lymphoma, and pheochromocytoma), chronic illnesses (chronic obstructive pulmonary disease and heart failure), physiological factors (menopause, pregnancy, and excessive heat), psychiatric conditions (anxiety), and neurological disorders (stroke, syringomyelia, and Parkinson's disease). Additionally, antidepressants, cholinergic agonists, and hypoglycemic drugs may contribute to the development of this condition (Table 1) [10–13].

Table 1

Causes of secondary hyperhidrosis [10–13]
Causes of Secondary Hyperhidrosis
Endocrine/metabolic disorders	diabetes mellitus, hyperthyroidism, hyperaldosteronism, acromegaly
Febrile illness/infection	defervescence, tuberculosis, bacteremia, malaria, brucellosis, HIV
Malignancies	carcinoid syndrome, pheochromocytoma, lymphoma
Chronic illness	chronic obstructive pulmonary disease, heart failure
Physiologic	menopause, autonomous nervous system dysfunction, pregnancy, heat
Psychiatric	generalized anxiety disorder, social anxiety
Substance abuse	alcohol, cocaine, amphetamine, narcotic withdrawal
Drugs	antidepressants (SSRI, SNRI) cholinergic agonists (bethanechol, pilocarpine, pyridostigmine) hypoglycemics (insulin, sulfonylurea, thiazolidinediones) SERM (raloxifene, tamoxifen) NSAIDs, antiemetics antibiotics (ciprofloxacin), antivirals (acyclovir) miscellaneous (infliximab, niacin, sildenafil)
Neurologic
Cortical condition	congenital autonomic dysfunction familial dysautonomia congenital ichthyosiform erythroderma encephalitis
Hypothalamic condition	hyperpituitarism, hypothalamic mass, Parkinson's disease, stroke, CVA, TIA
Medullary, spinal condition	auriculotemporal syndrome post-traumatic (spinal cord transaction or thoracic sympathetic chain injury), syringomyelia

CVA - Cerebrovascular Accident; HIV - Human Immunodeficiency Virus; NSAIDs - Nonsteroidal Anti-inflammatory Drugs; SERM - Selective Estrogen Receptor Modulator; SNRI - Serotonin-Norepinephrine Reuptake Inhibitor; SSRI - Selective Serotonin Reuptake Inhibitor; TIA - Transient Ischemic Attack

Trauma can also trigger hyperhidrosis. Frey syndrome, also known as auriculotemporal syndrome, is an aberrant reinnervation caused by injury to the auriculotemporal nerve, that most commonly occurs after parotidectomy but can also be a complication of facial fracture/joint injury repair, neck lymph node dissection, or infection and trauma to the parotid region [14]. According to Khurana, injury to the forehead with a hematoma may cause headaches, chronic ipsilateral ptosis, miosis, and hyperhidrosis [15]. Adams et al. reported a case of pediatric spinal cord injury from C7 to T3 that led to profound hyperhidrosis postoperatively after laminectomy [16]. Additionally, Glasauer et al. presented a case of a cervical spine fracture at C5, 6 that induced hyperhidrosis only when sitting upright and was relieved in the recumbent position [17]. Furthermore, Jang et al. reported a case of injury to the hypothalamus, the area that manages sweating, provoking hyperhidrosis [18].

Treatment of hyperhidrosis can be based on the resolution of the underlying cause or symptomatic management. Symptomatic management may focus on reducing the ability to sweat or deplete bodily fluids. Focal hyperhidrosis can be managed by eliminating glands themselves, such as through alcohol sclerosing or botulinum intoxication, which cannot be performed on the entire body. Moreover, generalized hyperhidrosis requires center-targeted therapy, such as systemic anticholinergic agents, ganglion nerve block, or hypo-modulation of the hypothalamus. Finally, surgical treatment is recommended when conservative treatment fails [19].

A 53-year-old male was transported to the Emergency Department of Korea University Anam Hospital in Seoul. He was involved in a motor-vehicle collision at 40 km/h. The helmet was damaged, revealing two lacerations on the forehead. He complained of pain in both thighs and had multiple bruises and abrasions on both lower extremities. He recalled losing consciousness for several minutes after the collision. The patient arrived with a fixed cervical spine, and the wound was covered.

The patient had underlying medical conditions such as hypertension, diabetes mellitus, chronic kidney disease, Hepatitis C, and angina. He underwent percutaneous coronary intervention stent insertion in 2016, pan-retinal laser coagulation for diabetic retinopathy in both eyes in 2021, and arteriovenous fistula construction for hemodialysis in 2021.

Upon arrival, his vital signs were stable, his mental status was alert, and the focused abdominal sonography in trauma was negative. No significant hemorrhage or fracture was visible on simple radiography or computed tomography of the abdominopelvic region, chest, or brain. The lacerations on the left tibia and right forehead were sutured in the Emergency Room. The Plastic Surgery department planned delayed primary closure with a local flap for the right forehead laceration as well as incision and drainage of the eyebrow hematoma. On the third day of admission, he began sweating unpleasantly. He had to change clothes several times daily because of excessive sweating (Figure 1). Moreover, he complained of chills, headache, and increased thirst. Symptoms were relieved only after hemodialysis but recurred the next day (Figure 2). Therefore, several tests were conducted to evaluate the potential causes (Table 2). As noted in (Table 1), hyperhidrosis can be triggered by either chronic or acute causes. In this case, the patient’s symptoms began after the accident; therefore, we mainly focused on acute causes. However, all radiological, serological, and psychological tests were negative. Brain and spine imaging revealed no evidence of bleeding or trauma. Laboratory test results and imaging of endocrinological abnormalities were normal. Bacterial cultures and laboratory tests for signs of infection yielded negative results. Furthermore, psychiatric survey results were normal, and autonomic function tests were not indicative of his symptoms. Transthoracic echocardiography and electrocardiography were performed to check for cholinergic crisis; however, they were unrelated to cholinergic toxicity, and vital signs were normal (Table 2).

Table 2. Assessment of hyperhidrosis
Differential diagnosis
Modality	Result
Central structural lesion
Brain MRI, CT	No microbleeding or traumatic damage
Endocrinological abnormalities (eg. Pheochromocytoma, hyperthyroidism, hyperaldosteronism)
APCT	no adrenal lesion
Lab	metanephrine, norepinephrine, dopamine normal or mildly elevated. ACTH mildly elevated, cortisol, aldosterone, TSH normal
Bacteremia
Culture	Forehead laceration culture: ADM 5 Pseudomonas monteilii Blood culture: ADM 6 Staphylococcus epidermidis - negative after ADM 12
Lab	Procalcitonin 0.13 (ADM 1) 7.07 (ADM 13) 0.181 (ADM 36) ng/mL CRP 2.37 (ADM 1) 8.03 (ADM 4) 2.20 (ADM 9) 25.57 (ADM 11) 3.23 (ADM 16) 1.93 (ADM 18) mg/L
TB
PCR, culture	negative
Autonomic nervous system abnormality
K-COMPASS (composite autonomic symptom score)	31 (no other symptom than cold sweating)
Autonomic function test (QSART)	delayed orthostatic hypotension, parasympathetic dysfunction, increased sweat secretion
Cord injury
Spine MRI, CT	inflammatory spondyloarthropathy, disc bulgings, neural foramen stenosis No remarkable cords signal changes nor enhancement No spinal fracture
Hypoglycemia
Blood sugar	WNL
Psychiatric cause
HADS (Hospital anxiety and depression scale) BDI (Beck depression inventory test)	normal
Cardiovascular
Transthoracic Echocardiography	Left ventricular (LV) eccentric hypertrophy, LV and atrial enlargement, prominent trabeculation at the LV apex, no regional wall motion abnormality of LV, low normal LV ejection fraction (54%), small amount of pericardial effusion (right ventricle side), Chiari network in the right atrium, mild tricuspid regurgitation, moderate pulmonary hypertension, thickened aortic valve and mitral valve
Electrocardiogram	Sinus rhythm, incomplete left bundle branch block, left ventricular hypertrophy, anterior infarct, possibly acute

ACTH - Adrenocorticotropic Hormone; ADM – Admission; APCT - Abdominopelvic Computed Tomography; BDI - Beck Depression Inventory; CRP - C-reactive Protein; CT - Computed Tomography; HADS - Hospital Anxiety and Depression Scale; K-COMPASS - Composite Autonomic Symptom Score; LV - Left Ventricle; MRI - Magnetic Resonance Imaging; PCR - Polymerase Chain Reaction; QSART - Quantitative Sudomotor Axon Reflex Test; TSH - Thyroid-stimulating Hormone; WNL - Within Normal Limits

Table 3. Symptomatic treatment and results
Treatment	Expectation	Result
Amitriptyline (TCA)	Anticholinergic effect	no effect
Sympathetic ganglion block (mepivacaine) at ADM 27, 28, 29, 33, 35	Suppress overactive sympathetic tone	no effect

TCA - Tricyclic Antidepressant

Ineluctably, we initiated symptomatic management without identifying the cause (Table 3). Initially, the patient showed an improvement in symptoms following sympathetic ganglion blockade; however, the symptoms recurred the following day. Several more blockades were administered, yet their effectiveness varied each time. Initially, the treatment seemed to have only a temporary effect; later observations revealed that symptom resolution occurred exclusively on the hemodialysis days. He also tried amitriptyline, anticipating its anticholinergic effects, following consultation with the Neurology Department; however, it proved ineffective.

Next, we assessed his weight change to determine if symptom improvement correlated with achieving an adequate dry-weight. His recorded height was 172 cm, and the Nephrology Department recommended a dry weight of 68.3 kg, revised from previous estimates of 69.5 and 68.5 kg due to early-detected cardiomegaly on chest radiography. Upon admission, his weight was 68.7 kg, which rose to 72.5 kg with ADM 14. Subsequently, following ADM 25, his weight stabilized between 66 and 69 kg, with ultrafiltration generally maintained at 0 ml, except on some occasions when it reached up to 800 mL (Figure 3). However, despite his dry body volume, he continued to experience excessive sweating. Moreover, the effectiveness of hemodialysis in alleviating his symptoms was evident. To evaluate the effectiveness of hemodialysis, we reviewed laboratory data prior to each session. His results consistently indicated significantly elevated blood urea nitrogen, creatinine, potassium, and phosphorus levels typical of chronic kidney disease, with these elevations largely mitigated following hemodialysis. The osmolality was calculated using the formula:

*** Osmolality = (2 × Na) + (blood urea nitrogen / 2.8) + (glucose / 18).

They were persistently high, and although not significantly, they were relieved after hemodialysis.

Prior to admission, the patient’s daily medications included: torsemide: 2.5 mg, losartan 100 mg, amlodipine 5 mg, carvedilol 6.25 mg, teneligliptin 20 mg, rosuvastatin 10 mg, nifedipine 30 mg, vitamin supplements QD, polystyrene sulfonate calcium 5 g BID, and sevelamer carbonate 800 mg TID, primarily for cardiologic and nephrologic conditions. For enhanced bowel and urinary function, the followings were administered: magnesium hydroxide 500 mg BID, motilitone (Coridalis tuber, Pharbitis seed) 30 mg, bethanechol 25 mg TID, and tamsulosin 0.2 mg HS. These additional medications were discontinued upon discharge.

Fortunately, the patient’s excessive sweating ceased three days after discharge. He no longer had to shower or change clothes several times. No further laboratory or imaging tests were performed. The patient remained dry for 10 months.

We conducted numerous tests to identify the probable causes of hyperhidrosis, all of which yielded normal results. Initially, certain symptomatic treatments appeared effective; however, we ultimately determined that hemodialysis was the sole method that alleviated the patient's symptoms. Many previous studies have explored the relationship between hemodialysis and diaphoresis. Hanafusa et al. noted that in chronic kidney disease/end-stage kidney disease patients, diaphoresis therapy can significantly enhance the cutaneous elimination of water, urea, lactate, sulfate, and electrolytes such as sodium, potassium, and chloride [20]. Furthermore, Maggiani-Aguilera et al. demonstrated that portable sauna bath-induced diaphoresis is an effective alternative method for managing fluid overload in patients with chronic kidney disease [21]. Additionally, Fortney et al. observed that upon the initiation of sweating, at the same rise in internal temperature, the increase in sweating was lesser when individuals were hypovolemic but iso-osmotic, whereas hypervolemic individuals exhibited significantly more sweating than controls during exercise [22]. In our case, we initially speculated that the patient's symptoms were due to volume overload, which seemed to resolve post-dialysis owing to volume reduction. However, the symptoms persisted even after the patient reached his dry weight (Fig. 3). Notably, pre-hemodialysis laboratory results were generally unremarkable, except for an increase in osmolality during admission compared to the first day. Although this increase was not substantial, it was partially resolved following hemodialysis (Table 4). However, according to a study by Fortney et al., individuals with hyperosmolarity exhibited a significantly higher internal temperature threshold for the onset of sweating compared to those in iso-osmotic conditions [23], suggesting that hyperosmolarity should have reduced sweat, yet this does not account for the observed decrease in sweating post-hemodialysis.

Although the magnetic resonance imaging scans of the brain and spinal cord did not exhibit meaningful findings, as the symptoms initiated after the traffic accident, trauma to the hypothalamic region or spinal cord was initially suspected. However, imaging features of subtle hypothalamic injuries may not be observed in the immediate post-traumatic stage [24]. We recommended follow-up with imaging modalities, but the patient later refused because his symptoms had stopped.

During admission, magnesium and motilitone (5-HTa receptor agonist, Da receptor antagonist) were prescribed in addition to his daily medication to improve bowel movement, and bethanechol and tamsulosin were prescribed to improve bladder function. Bethanecol is an acetylcholine analog that is resistant to cholinesterase inactivation. When overdosed, cholinergic toxicity must be monitored as untreated cholinergic toxicity may result in death with an estimated 15% fatality rate [25]. It is primarily metabolized in the liver and excreted by the kidneys. However, patients with end-stage kidney disease lack guidelines for reduced dosage [26]. Bruno Correia Jham et al. conducted a randomized prospective stage III trial on bethanechol administration to prevent radiotherapy-induced salivary gland damage, where two out of 22 patients who were administered bethanechol reported sweating as a side effect [27]. Gorsky et al. evaluated the efficacy of bethanechol, and found that three out of 37 patients (8.1%) complained of excessive sweating [29]. In our case, the patient ceased bethanechol following discharge, and symptoms resolved within three days. He also experienced increased thirst and water intake. While previously consuming an average of 500 mL/day until the 15th day, his water intake subsequently increased, frequently exceeding 1000 mL/day and reaching up to 1800 mL/day at its peak. Melvin et al. observed a bethanechol-induced increase in water intake in rats [28]. Levy Erez documented two cases of bethanechol-induced hyperhidrosis [26]. A 65-year-old male with acute urinary retention was treated with bethanechol and developed profuse sweating, hypersialorrhea, and polydipsia; four days later, all symptoms resolved post-cessation of bethanechol administration. A 59-year-old female also suffering from urinary retention started bethanechol and developed profuse sweating, hypersialorrhea, and gastrointestinal distress, which resolved within 24 h of stopping the medication [26].

The relationship between the initiation and cessation of bethanechol and the symptoms raises the possibility of drug-induced hyperhidrosis. However, diaphoresis is not a common side effect of bethanechol, occurring in only 8–10% of cases. Notably, the fact that the symptom showed no response to the anticholinergic amitriptyline, and only responded to hemodialysis, strongly opposes the idea.

A 53-year-old man was admitted to the hospital for 52 days after sustaining injuries in a traffic accident. Treatment included delayed suturing of the forehead laceration on ADM 8. Subsequently, he remained hospitalized for an additional 44 days to address persistent sweating issues. Remarkably, his symptoms, which showed no response to any tests or treatments, abated as soon as he was discharged. The patient's condition was a case of hyperhidrosis triggered by trauma, whose cause remained elusive in etiology but unexpectedly resolved following hemodialysis.

ACTH

Adrenocorticotropic Hormone

ADM

Admission

APCT

Abdominopelvic Computed Tomography

AST

Aspartate Aminotransferase

ALT

Alanine Aminotransferase

ALP

Alkaline Phosphatase

BID

Bis in die (Twice a day)

BDI

Beck Depression Inventory

BUN

Blood Urea Nitrogen

CVA

Cerebrovascular Accident

Cr

Creatinine

CRP

C-reactive Protein

CT

Computed Tomography

HADS

Hospital Anxiety and Depression Scale

HD

Hemodialysis

HS

Hora Somni

HIV

Human Immunodeficiency Virus

K

COMPASS-Composite Autonomic Symptom Score

LV

Left Ventricle

MRI

Magnetic Resonance Imaging

NSAIDs

Nonsteroidal Anti-inflammatory Drugs

PCR

Polymerase Chain Reaction

QID

Quarter in die (Four times a day)

QSART

Quantitative Sudomotor Axon Reflex Test

SERM

Selective Estrogen Receptor Modulator

SNRI

Serotonin-Norepinephrine Reuptake Inhibitor

SSRI

Selective Serotonin Reuptake Inhibitor

TCA

Tricyclic Antidepressant

TIA

Transient Ischemic Attack

TID

Ter in die (Three times a day)

TSH

Thyroid-stimulating Hormone

Ethics approval and consent to participate
The patient provided verbal and written consent for this work, and as this is a case report describing clinical observations, ethics approval was waived.

Consent for publication
Written informed consent was obtained from the case patient for publication of this report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.

Competing interests

The authors declare no conflicts of interest.

Funding

No external funding received to conduct this study.

Author Contribution

YP conceived the study and carried out the clinical research. HP and YP participated in the design of the manuscript. All authors participated in the revision of the manuscript and table. All authors read and approved the final manuscript.

Acknowledgement

We would like to thank the patient for contributing information for this letter.

Availability of data and materials

All data related to this case report are documented within this manuscript.

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Table 4 is available in the Supplementary Files section.

No competing interests reported.

Table4.docx

Idiopathic Hyperhidrosis after Trauma: A Case Report

Status:

Version 1

Abstract

Figures

BACKGROUND

CASE PRESENTATION

DISCUSSION and CONCLUSIONS

Abbreviations

Declarations

Ethics approval and consent to participate
The patient provided verbal and written consent for this work, and as this is a case report describing clinical observations, ethics approval was waived.

Consent for publication
Written informed consent was obtained from the case patient for publication of this report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.

Competing interests

Funding

Author Contribution

Acknowledgement

Availability of data and materials

References

Tables

Additional Declarations

Supplementary Files

Status:

Version 1

Idiopathic Hyperhidrosis after Trauma: A Case Report

Status:

Version 1

Abstract

Figures

BACKGROUND

CASE PRESENTATION

DISCUSSION and CONCLUSIONS

Abbreviations

Declarations

Ethics approval and consent to participate The patient provided verbal and written consent for this work, and as this is a case report describing clinical observations, ethics approval was waived.

Consent for publication Written informed consent was obtained from the case patient for publication of this report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.

Competing interests

Funding

Author Contribution

Acknowledgement

Availability of data and materials

References

Tables

Additional Declarations

Supplementary Files

Status:

Version 1

Ethics approval and consent to participate
The patient provided verbal and written consent for this work, and as this is a case report describing clinical observations, ethics approval was waived.

Consent for publication
Written informed consent was obtained from the case patient for publication of this report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.