Emergency Medicine

ANSWER
Several findings are evident from this radiograph. First, the quality is slightly diminished due to the patient’s size and artifact from the backboard. The patient’s mediastinum is somewhat widened, which is concerning for possible occult chest/vascular injury. There is some haziness within the left apical region suggestive of a hemothorax; no definite pneumothorax is seen. The left clavicle is fractured and displaced, and the left scapula is fractured as well.

ANSWER
Several findings are evident from this radiograph. First, the quality is slightly diminished due to the patient’s size and artifact from the backboard. The patient’s mediastinum is somewhat widened, which is concerning for possible occult chest/vascular injury. There is some haziness within the left apical region suggestive of a hemothorax; no definite pneumothorax is seen. The left clavicle is fractured and displaced, and the left scapula is fractured as well.

ANSWER
Several findings are evident from this radiograph. First, the quality is slightly diminished due to the patient’s size and artifact from the backboard. The patient’s mediastinum is somewhat widened, which is concerning for possible occult chest/vascular injury. There is some haziness within the left apical region suggestive of a hemothorax; no definite pneumothorax is seen. The left clavicle is fractured and displaced, and the left scapula is fractured as well.

Study Overview

Objective. To compare rates of asthma action plan use in limited English proficiency (LEP) caregivers compared with English proficient (EP) caregivers.

Design. Cross-sectional survey.

Participants and setting. A convenience sample of 107 Latino caregivers of children with asthma at an urban academic emergency department (ED). Surveys in the preferred language of the patient (English or Spanish, with the translated version previously validated) were distributed at the time of the ED visit. Interpreters were utilized when requested.

Main outcome measure. Caregiver use of an asthma action plan.

Main results. 51 LEP caregivers and 56 EP caregivers completed the survey. Mothers completed the surveys 87% of the time and the average age of patients was 4 years.  Among the EP caregivers, 64% reported using an asthma action plan, while only 39% of the LEP caregivers reported using one. The difference was statistally significant (P = 0.01). Through both correlations and regressions, English proficiency was the only variable (others included health insurance status and level of caregiver education) that showed a significant effect on asthma action plan use.

Conclusions. Children whose caregiver had LEP were significantly less likely to have and use an asthma action plan. Asthma education in the language of choice of the patient may help improve asthma care.

Commentary

With 20% of US households now speaking a language other than English at home [1], language barriers between providers and patients present multiple challenges to health services delivery and can significantly contribute to immigrant health disparities. Despite US laws and multiple federal agency policies requiring the use of interpreters during health care encounters, organizations continue to fall short of providing interpreter services and often lack adequate or equivalent materials for patient education. Too often, providers overestimate their language skills [2,3], use colleagues as ad hoc interpreters out of convenience [4], or rely on family members for interpretation [4]—a practice that is universally discouraged.

Recent research does suggest that the timing of interpreter use is critical. In planned encounters such as primary care visits, interpreters can and should be scheduled for visits when a language-concordant provider is not available. During hospitalizations, including ED visits, interpreters are most effective when used on admission, during patient teaching, and upon discharge, and the timing of these visits has been shown to affect length of stay and readmission rates [5,6].

This study magnifies the consequences of failing to provide language-concordant services to patients and their caregivers. It also helps to identify one of the sources of pediatric asthma health disparities in Latino populations. The emphasis on the role of the caregiver in action plan utilization is a unique aspect of this study and it is one of the first to examine the issue in this way. It highlights the importance of caregivers in health system transitions and illustrates how a language barrier can potentially impact transitions.

The authors’ explicit use of a power analysis to calculate their sample size is a strength of the study. Furthermore, the authors differentiated their respondents by country of origin, something that rarely occurs in studies of Latinos [7], and allows the reader to differentiate the impact of the intervention at a micro level within this population. The presentation of Spanish language quotes with their translations within the manuscript provides transparency for bilingual readers to verify the accuracy of the authors’ translation.

There are, however, a number of methodological issues that should be noted. The authors acknowledge that they did not account for asthma severity in the survey nor control for it in the analysis, did not assess health literacy, and did not differentiate their results based on country of origin. The latter point is important because the immigration experience and demographic profiles of Latinos differs significantly by country of origin and could factor in to action plan use. The translation process used for survey instrument translation also did not illustrate how it accounted for the well-established linguistic variation that occurs in the Spanish language. Additionally, US census data shows that the main countries of origin of Latinos in the service area of the study are Puerto Rico, Ecuador, and Mexico [1]. The survey itself had Ecuador as a write in and Dominican as a response option. The combination presented in the survey reflects the Latino demographic composition in the nearest large urban area. Thus, when collecting country of origin data on immigrant patients, country choices should reflect local demographics and not national trends for maximum precision.

Another concern is that Spanish language literacy was not assessed. Many Latino immigrants may have limited reading ability in Spanish. For Mexican immigrants in particular, Spanish may be a second language after their indigenous language. This is also true for some South American Latino immigrants from the Andean region. Many Latino immigrants come to the United States with less than an 8th grade education and likely come from educational systems of poor quality, which subsequently affects their Spanish language reading and writing skills [8]. Assessing education level based on US equivalents is not an accurate way to gauge literacy. Thus, assessing reading literacy in Spanish before surveying patients would have been a useful step that could have further refined the results. These factors will have implications for action plan utilization and implementation for any chronic disease.

Providers often think that language barriers are an obvious factor in health disparities and service delivery, but few studies have actually captured or quantified the effects of language barriers on health outcomes. Most studies only identify language barriers as an access issue. This study provides a good illustration of the impact of a language barrier on a known and effective intervention for pediatric asthma management. Practitioners can take the consequences illustrated in this study and easily extrapolate the contribution to health disparities on a broader scale.

Applications for Clinical Practice

Practitioners caring for patients in EDs where the patient or caregiver has a language barrier should make every effort to use appropriate interpreter services when patient teaching occurs. Assessing not only for health literacy but reading ability in the LEP patient or caregiver is also important, since it will affect dyad’s ability to implement self-care measures recommended in patient teaching sessions or action plan implementation. Asking the patient what their country of origin is, regardless of their legal status, will help practitioners refine patient teaching and the language they (and the interpreter when appropriate) use to illustrate what needs to be done to manage their condition.

—Allison Squires, PhD, RN

Study Overview

Objective. To compare rates of asthma action plan use in limited English proficiency (LEP) caregivers compared with English proficient (EP) caregivers.

Design. Cross-sectional survey.

Participants and setting. A convenience sample of 107 Latino caregivers of children with asthma at an urban academic emergency department (ED). Surveys in the preferred language of the patient (English or Spanish, with the translated version previously validated) were distributed at the time of the ED visit. Interpreters were utilized when requested.

Main outcome measure. Caregiver use of an asthma action plan.

Main results. 51 LEP caregivers and 56 EP caregivers completed the survey. Mothers completed the surveys 87% of the time and the average age of patients was 4 years.  Among the EP caregivers, 64% reported using an asthma action plan, while only 39% of the LEP caregivers reported using one. The difference was statistally significant (P = 0.01). Through both correlations and regressions, English proficiency was the only variable (others included health insurance status and level of caregiver education) that showed a significant effect on asthma action plan use.

Conclusions. Children whose caregiver had LEP were significantly less likely to have and use an asthma action plan. Asthma education in the language of choice of the patient may help improve asthma care.

Commentary

With 20% of US households now speaking a language other than English at home [1], language barriers between providers and patients present multiple challenges to health services delivery and can significantly contribute to immigrant health disparities. Despite US laws and multiple federal agency policies requiring the use of interpreters during health care encounters, organizations continue to fall short of providing interpreter services and often lack adequate or equivalent materials for patient education. Too often, providers overestimate their language skills [2,3], use colleagues as ad hoc interpreters out of convenience [4], or rely on family members for interpretation [4]—a practice that is universally discouraged.

Recent research does suggest that the timing of interpreter use is critical. In planned encounters such as primary care visits, interpreters can and should be scheduled for visits when a language-concordant provider is not available. During hospitalizations, including ED visits, interpreters are most effective when used on admission, during patient teaching, and upon discharge, and the timing of these visits has been shown to affect length of stay and readmission rates [5,6].

This study magnifies the consequences of failing to provide language-concordant services to patients and their caregivers. It also helps to identify one of the sources of pediatric asthma health disparities in Latino populations. The emphasis on the role of the caregiver in action plan utilization is a unique aspect of this study and it is one of the first to examine the issue in this way. It highlights the importance of caregivers in health system transitions and illustrates how a language barrier can potentially impact transitions.

The authors’ explicit use of a power analysis to calculate their sample size is a strength of the study. Furthermore, the authors differentiated their respondents by country of origin, something that rarely occurs in studies of Latinos [7], and allows the reader to differentiate the impact of the intervention at a micro level within this population. The presentation of Spanish language quotes with their translations within the manuscript provides transparency for bilingual readers to verify the accuracy of the authors’ translation.

There are, however, a number of methodological issues that should be noted. The authors acknowledge that they did not account for asthma severity in the survey nor control for it in the analysis, did not assess health literacy, and did not differentiate their results based on country of origin. The latter point is important because the immigration experience and demographic profiles of Latinos differs significantly by country of origin and could factor in to action plan use. The translation process used for survey instrument translation also did not illustrate how it accounted for the well-established linguistic variation that occurs in the Spanish language. Additionally, US census data shows that the main countries of origin of Latinos in the service area of the study are Puerto Rico, Ecuador, and Mexico [1]. The survey itself had Ecuador as a write in and Dominican as a response option. The combination presented in the survey reflects the Latino demographic composition in the nearest large urban area. Thus, when collecting country of origin data on immigrant patients, country choices should reflect local demographics and not national trends for maximum precision.

Another concern is that Spanish language literacy was not assessed. Many Latino immigrants may have limited reading ability in Spanish. For Mexican immigrants in particular, Spanish may be a second language after their indigenous language. This is also true for some South American Latino immigrants from the Andean region. Many Latino immigrants come to the United States with less than an 8th grade education and likely come from educational systems of poor quality, which subsequently affects their Spanish language reading and writing skills [8]. Assessing education level based on US equivalents is not an accurate way to gauge literacy. Thus, assessing reading literacy in Spanish before surveying patients would have been a useful step that could have further refined the results. These factors will have implications for action plan utilization and implementation for any chronic disease.

Providers often think that language barriers are an obvious factor in health disparities and service delivery, but few studies have actually captured or quantified the effects of language barriers on health outcomes. Most studies only identify language barriers as an access issue. This study provides a good illustration of the impact of a language barrier on a known and effective intervention for pediatric asthma management. Practitioners can take the consequences illustrated in this study and easily extrapolate the contribution to health disparities on a broader scale.

Applications for Clinical Practice

Practitioners caring for patients in EDs where the patient or caregiver has a language barrier should make every effort to use appropriate interpreter services when patient teaching occurs. Assessing not only for health literacy but reading ability in the LEP patient or caregiver is also important, since it will affect dyad’s ability to implement self-care measures recommended in patient teaching sessions or action plan implementation. Asking the patient what their country of origin is, regardless of their legal status, will help practitioners refine patient teaching and the language they (and the interpreter when appropriate) use to illustrate what needs to be done to manage their condition.

—Allison Squires, PhD, RN

Study Overview

Objective. To compare rates of asthma action plan use in limited English proficiency (LEP) caregivers compared with English proficient (EP) caregivers.

Design. Cross-sectional survey.

Participants and setting. A convenience sample of 107 Latino caregivers of children with asthma at an urban academic emergency department (ED). Surveys in the preferred language of the patient (English or Spanish, with the translated version previously validated) were distributed at the time of the ED visit. Interpreters were utilized when requested.

Main outcome measure. Caregiver use of an asthma action plan.

Main results. 51 LEP caregivers and 56 EP caregivers completed the survey. Mothers completed the surveys 87% of the time and the average age of patients was 4 years.  Among the EP caregivers, 64% reported using an asthma action plan, while only 39% of the LEP caregivers reported using one. The difference was statistally significant (P = 0.01). Through both correlations and regressions, English proficiency was the only variable (others included health insurance status and level of caregiver education) that showed a significant effect on asthma action plan use.

Conclusions. Children whose caregiver had LEP were significantly less likely to have and use an asthma action plan. Asthma education in the language of choice of the patient may help improve asthma care.

Commentary

With 20% of US households now speaking a language other than English at home [1], language barriers between providers and patients present multiple challenges to health services delivery and can significantly contribute to immigrant health disparities. Despite US laws and multiple federal agency policies requiring the use of interpreters during health care encounters, organizations continue to fall short of providing interpreter services and often lack adequate or equivalent materials for patient education. Too often, providers overestimate their language skills [2,3], use colleagues as ad hoc interpreters out of convenience [4], or rely on family members for interpretation [4]—a practice that is universally discouraged.

Recent research does suggest that the timing of interpreter use is critical. In planned encounters such as primary care visits, interpreters can and should be scheduled for visits when a language-concordant provider is not available. During hospitalizations, including ED visits, interpreters are most effective when used on admission, during patient teaching, and upon discharge, and the timing of these visits has been shown to affect length of stay and readmission rates [5,6].

This study magnifies the consequences of failing to provide language-concordant services to patients and their caregivers. It also helps to identify one of the sources of pediatric asthma health disparities in Latino populations. The emphasis on the role of the caregiver in action plan utilization is a unique aspect of this study and it is one of the first to examine the issue in this way. It highlights the importance of caregivers in health system transitions and illustrates how a language barrier can potentially impact transitions.

The authors’ explicit use of a power analysis to calculate their sample size is a strength of the study. Furthermore, the authors differentiated their respondents by country of origin, something that rarely occurs in studies of Latinos [7], and allows the reader to differentiate the impact of the intervention at a micro level within this population. The presentation of Spanish language quotes with their translations within the manuscript provides transparency for bilingual readers to verify the accuracy of the authors’ translation.

There are, however, a number of methodological issues that should be noted. The authors acknowledge that they did not account for asthma severity in the survey nor control for it in the analysis, did not assess health literacy, and did not differentiate their results based on country of origin. The latter point is important because the immigration experience and demographic profiles of Latinos differs significantly by country of origin and could factor in to action plan use. The translation process used for survey instrument translation also did not illustrate how it accounted for the well-established linguistic variation that occurs in the Spanish language. Additionally, US census data shows that the main countries of origin of Latinos in the service area of the study are Puerto Rico, Ecuador, and Mexico [1]. The survey itself had Ecuador as a write in and Dominican as a response option. The combination presented in the survey reflects the Latino demographic composition in the nearest large urban area. Thus, when collecting country of origin data on immigrant patients, country choices should reflect local demographics and not national trends for maximum precision.

Another concern is that Spanish language literacy was not assessed. Many Latino immigrants may have limited reading ability in Spanish. For Mexican immigrants in particular, Spanish may be a second language after their indigenous language. This is also true for some South American Latino immigrants from the Andean region. Many Latino immigrants come to the United States with less than an 8th grade education and likely come from educational systems of poor quality, which subsequently affects their Spanish language reading and writing skills [8]. Assessing education level based on US equivalents is not an accurate way to gauge literacy. Thus, assessing reading literacy in Spanish before surveying patients would have been a useful step that could have further refined the results. These factors will have implications for action plan utilization and implementation for any chronic disease.

Providers often think that language barriers are an obvious factor in health disparities and service delivery, but few studies have actually captured or quantified the effects of language barriers on health outcomes. Most studies only identify language barriers as an access issue. This study provides a good illustration of the impact of a language barrier on a known and effective intervention for pediatric asthma management. Practitioners can take the consequences illustrated in this study and easily extrapolate the contribution to health disparities on a broader scale.

Applications for Clinical Practice

Practitioners caring for patients in EDs where the patient or caregiver has a language barrier should make every effort to use appropriate interpreter services when patient teaching occurs. Assessing not only for health literacy but reading ability in the LEP patient or caregiver is also important, since it will affect dyad’s ability to implement self-care measures recommended in patient teaching sessions or action plan implementation. Asking the patient what their country of origin is, regardless of their legal status, will help practitioners refine patient teaching and the language they (and the interpreter when appropriate) use to illustrate what needs to be done to manage their condition.

—Allison Squires, PhD, RN

ANSWER

The image shows a comminuted and depressed fracture of the lateral tibial plateau. It is depressed approximately 6 to 7 mm. The patient was admitted, and orthopedic consultation was obtained. The patient subsequently underwent an open reduction and internal fixation of the fracture.

ANSWER

The image shows a comminuted and depressed fracture of the lateral tibial plateau. It is depressed approximately 6 to 7 mm. The patient was admitted, and orthopedic consultation was obtained. The patient subsequently underwent an open reduction and internal fixation of the fracture.

ANSWER

The image shows a comminuted and depressed fracture of the lateral tibial plateau. It is depressed approximately 6 to 7 mm. The patient was admitted, and orthopedic consultation was obtained. The patient subsequently underwent an open reduction and internal fixation of the fracture.

A 26-year-old man presented to the emergency department (ED) with a chief complaint of abdominal pain. After triage was complete, he was transported to an examination room, where the clinician obtained the history of presenting illness. The onset of pain was approximately 90 minutes prior to arrival at the ED and woke the patient from a “sound sleep.”  He stated that the pain initially started as a “3 out of 10” but had progressed to a “12 out of 10,” and he described it as being in the right lower quadrant of his abdomen, with radiation to his right testicle. However, he was unsure where the pain started or if it was worse in either location. Nausea was the primary associated symptom, but he denied vomiting, diarrhea, fever, dysuria, or hematuria. Last, the patient denied history of trauma.   

Medical history was noncontributory: He denied previous gastrointestinal diseases, and there was no history of renal stones, urinary tract infection, or any other genitourinary disease. He had no surgical history. The patient smoked less than a pack of cigarettes per day but denied alcohol or drug use.

Physical examination revealed a young man in moderate discomfort. Despite describing his pain as a “12 out of 10,” he had a blood pressure of 121/72 mm Hg; pulse, 59 beats/min; respiratory rate, 20 breaths/min; and temperature, 96.8°F. HEENT and cardiovascular, respiratory, musculoskeletal, and neurologic exam results were all within normal limits. Abdominal examination revealed a mildly tender right lower quadrant with deep palpation, but no rebound or guarding. Murphy sign was negative.

Because of the complaint of pain radiating to the testicles, a genitourinary examination was performed. The penis appeared unremarkable, with no lesions or discharge. There was no inguinal lymphadenopathy. The scrotum appeared appropriate in size and was also grossly unremarkable. The left testicle was nontender. However, palpation of the right testicle elicited moderate to severe pain. There was no visible swelling, and there were no palpable hernias or other masses. Cremasteric reflex was assessed bilaterally and deemed to be absent on the right side.

A workup was initiated that included a complete blood count, comprehensive metabolic panel, and urinalysis; the results of these tests were unremarkable. A differential diagnosis was formed, with emphasis on appendicitis and testicular torsion. Because of the specific nature and location of the pain, both ultrasound and CT of the abdomen/pelvis were considered. It was decided to order the ultrasound, with a plan to perform CT only if ultrasound was unremarkable. The patient was medicated for his pain and the ultrasound commenced. Halfway through the imaging, the clinician and attending physician were summoned to the examination room to review the image seen in Figure 1.

On the next page: Discussion and diagnosis >>

DISCUSSION

Testicular torsion may occur if the testicle twists or rotates on the spermatic cord. The twisting causes arterial ischemia and venous outflow obstruction, cutting off the testicle’s blood supply.^1,2 Torsion may be extravaginal or intravaginal, depending on the extent of involvement of the surrounding structures.²

Extravaginal torsion is most commonly seen in neonates and occurs because the entire testicle may freely rotate prior to fixation to the scrotal wall via the tunica vaginalis.²Intravaginal torsion is more common in adolescents and often occurs as a result of a condition known as bell clapper deformity. This congenital abnormality enables the testicle to rotate within the tunica vaginalis and rest transversely in the scrotum instead of in a more vertical orientation.^2,3 Torsion occurs if the testicle rotates 90° to 180°, with complete torsion occurring at 360° (torsion may extend to as much as 720°).² Torsion may also occur as a result of trauma.¹

Peak incidence of testicular torsion occurs at ages 13 to 14, but it can occur at any age; torsion affects approximately 1 in 4,000 males younger than 25.^2-5 Ninety-five percent of all torsions are intravaginal.² Torsion is the most common pathology for males who undergo surgical exploration for scrotal pain.³

The main goal in the diagnosis and treatment of torsion is testicular salvage. Torsion is considered a urologic emergency, making early diagnosis and treatment critical to prevent testicular loss. In fact, a review of the relevant literature reveals that the rate of testicular salvage is much higher if the diagnosis is made within 6 to 12 hours.^1,2,5 Potential sequelae from delayed treatment include testicular infarction, loss of testicle, infertility problems, infections, cosmetic deformity, and increased risk for testicular malignancy.²

Because many men hesitate to seek medical attention for symptoms of testicular pain and swelling, the primary care clinician should openly discuss testicular disorders, especially with preadolescent males, during testicular examinations.⁶

Diagnosis

A testicular examination should be performed on any male presenting with a chief complaint of lower abdominal pain, back/flank pain, or any pain that radiates to the groin. The cremasteric reflex should be assessed because it can help differentiate among the causes of testicular pain.⁷ It is performed by gently stroking the upper inner thigh and observing for contraction of the ipsilateral testicle. One study found that, in cases of torsion, the absence of a cremasteric reflex had a sensitivity of 96% and a specificity of 88%.⁷ See the Table for the differential diagnosis for acute testicular pain.

While it is often possible to make the diagnosis of testicular torsion clinically, ultrasound with color Doppler is the diagnostic test of choice in cases for which the cause of acute scrotal pain is unclear.⁸ Ultrasound provides anatomic detail of the scrotum and its contents, and perfusion is assessed by adding the color Doppler images.⁸ It is important to note that, while the absence of blood flow is considered diagnostic for testicular torsion, the presence of flow does not necessarily exclude it.⁴

On the next page: Treatment >>

Treatment

Surgical exploration with intraoperative detorsion and orchiopexy (fixation of the testicle to the scrotal wall) is the mainstay of treatment for testicular torsion.¹ Orchiopexy is often performed bilaterally in order to prevent future torsion of the unaffected testicle. In about 40% of males with the bell clapper deformity, the condition is present on both sides.² Orchiectomy, the complete removal of the testicle, is necessary when the degree of torsion and subsequent ischemia have caused irreversible damage to the testicle.⁶ In one study in which 2,248 cases of torsion were reviewed, approximately 34% of males required orchiectomy.⁶

If surgery may be delayed, the clinician may attempt manual detorsion at the bedside. Despite the “open book” method described in many texts—which instructs the practitioner to rotate the testicle laterally—a review of the literature reveals that torsion takes place medially only 70% of the time.^1,5 The clinician should always consider this when any attempts at manual detorsion are made and correlate his or her technique with physical examination and the patient’s response.⁵

Relief of pain and return of the testicle to its natural longitudinal lie are considered indicators of successful detorsion.¹ Color Doppler ultrasound should be used to confirm the return of circulation. However, in one case review of pediatric patients who underwent surgical exploration after manual detorsion, some degree of residual torsion remained in 32%.⁵ Because of this risk, surgery is still indicated even in cases of successful bedside detorsion.⁵

On the next page: Case continuation >> 

CASE CONTINUATION

The decision to perform bedside ultrasound was made because the diagnosis of testicular torsion is a surgical emergency, and the window of time to prevent complications can be extremely narrow. If the ultrasound had been normal, then a CT scan may have provided additional data on which to base the diagnosis.

The patient was given adequate parenteral pain medication. After color Doppler ultrasound confirmed the torsion, the testicle was laterally rotated approximately 360°. The patient reported alleviation of his symptoms. Color Doppler was again performed to confirm the return of hyperemic blood flow to the affected testicle (Figure 2). The urologist arrived shortly thereafter and the patient was taken to the operating room, where he underwent scrotal exploration and bilateral orchiopexy.

On the next page: Conclusion >>

CONCLUSION

A testicular examination should be performed on any male presenting with a chief complaint of lower abdominal pain, back/flank pain, or any pain that radiates to the groin. Testicular torsion is most commonly seen in infants and adolescents but can occur at any age. The condition is a surgical emergency and the goal is testicular salvage, which is most likely to occur before 12 hours have elapsed since the onset of symptoms. An important component of the physical examination is attempting to elicit the cremasteric reflex, which is likely to be absent in the presence of torsion.

The primary care provider’s goal is to rapidly diagnose testicular torsion, then refer the patient immediately to a urologist or ED. The skilled clinician may attempt manual detorsion, based on his/her expertise and comfort level; however, this procedure should never delay prompt surgical intervention.

REFERENCES

1. Eyre RC. Evaluation of the acute scrotum in adults. www.uptodate.com/contents/evaluation-of-the-acute-scrotum-in-adults. Accessed May 16, 2014.

2. Ogunyemi OI, Weiker M, Abel EJ. Testicular torsion. http://emedicine.medscape.com/article/2036003-overview. Accessed May 16, 2014.

3. Khan F, Muoka O, Watson GM. Bell clapper testis, torsion, and detorsion: a case report. Case Rep Urol. 2011;2011:631970.

4. Molokwu CN, Somani BK, Goodman CM. Outcomes of scrotal exploration for acute scrotal pain suspicious of testicular torsion: a consecutive case series of 173 patients. BJU Int. 2011;107(6):990-993.

5. Sessions AE, Rabinowitz R, Hulbert WC, et al. Testicular torsion: direction, degree, duration and disinformation. J Urol. 2003;169(2):663-665.

6. Mansbach JM, Forbes P, Peters C. Testicular torsion and risk factors for orchiectomy. Arch Pediatr Adolesc Med. 2005;159:1167-1171.

7. Schmitz D, Safranek S. How useful is a physical exam in diagnosing testicular torsion? J Fam Pract. 2009;58(8):433-434.

8. D’Andrea A, Coppolino F, Cesarano E, et al. US in the assessment of acute scrotum. Crit Ultrasound J. 2013;5(suppl 1):S8. www.criticalultrasound journal.com/content/5/S1/S8/. Accessed May 16, 2014.

A 26-year-old man presented to the emergency department (ED) with a chief complaint of abdominal pain. After triage was complete, he was transported to an examination room, where the clinician obtained the history of presenting illness. The onset of pain was approximately 90 minutes prior to arrival at the ED and woke the patient from a “sound sleep.”  He stated that the pain initially started as a “3 out of 10” but had progressed to a “12 out of 10,” and he described it as being in the right lower quadrant of his abdomen, with radiation to his right testicle. However, he was unsure where the pain started or if it was worse in either location. Nausea was the primary associated symptom, but he denied vomiting, diarrhea, fever, dysuria, or hematuria. Last, the patient denied history of trauma.   

Medical history was noncontributory: He denied previous gastrointestinal diseases, and there was no history of renal stones, urinary tract infection, or any other genitourinary disease. He had no surgical history. The patient smoked less than a pack of cigarettes per day but denied alcohol or drug use.

Physical examination revealed a young man in moderate discomfort. Despite describing his pain as a “12 out of 10,” he had a blood pressure of 121/72 mm Hg; pulse, 59 beats/min; respiratory rate, 20 breaths/min; and temperature, 96.8°F. HEENT and cardiovascular, respiratory, musculoskeletal, and neurologic exam results were all within normal limits. Abdominal examination revealed a mildly tender right lower quadrant with deep palpation, but no rebound or guarding. Murphy sign was negative.

Because of the complaint of pain radiating to the testicles, a genitourinary examination was performed. The penis appeared unremarkable, with no lesions or discharge. There was no inguinal lymphadenopathy. The scrotum appeared appropriate in size and was also grossly unremarkable. The left testicle was nontender. However, palpation of the right testicle elicited moderate to severe pain. There was no visible swelling, and there were no palpable hernias or other masses. Cremasteric reflex was assessed bilaterally and deemed to be absent on the right side.

A workup was initiated that included a complete blood count, comprehensive metabolic panel, and urinalysis; the results of these tests were unremarkable. A differential diagnosis was formed, with emphasis on appendicitis and testicular torsion. Because of the specific nature and location of the pain, both ultrasound and CT of the abdomen/pelvis were considered. It was decided to order the ultrasound, with a plan to perform CT only if ultrasound was unremarkable. The patient was medicated for his pain and the ultrasound commenced. Halfway through the imaging, the clinician and attending physician were summoned to the examination room to review the image seen in Figure 1.

On the next page: Discussion and diagnosis >>

DISCUSSION

Testicular torsion may occur if the testicle twists or rotates on the spermatic cord. The twisting causes arterial ischemia and venous outflow obstruction, cutting off the testicle’s blood supply.^1,2 Torsion may be extravaginal or intravaginal, depending on the extent of involvement of the surrounding structures.²

Extravaginal torsion is most commonly seen in neonates and occurs because the entire testicle may freely rotate prior to fixation to the scrotal wall via the tunica vaginalis.²Intravaginal torsion is more common in adolescents and often occurs as a result of a condition known as bell clapper deformity. This congenital abnormality enables the testicle to rotate within the tunica vaginalis and rest transversely in the scrotum instead of in a more vertical orientation.^2,3 Torsion occurs if the testicle rotates 90° to 180°, with complete torsion occurring at 360° (torsion may extend to as much as 720°).² Torsion may also occur as a result of trauma.¹

Peak incidence of testicular torsion occurs at ages 13 to 14, but it can occur at any age; torsion affects approximately 1 in 4,000 males younger than 25.^2-5 Ninety-five percent of all torsions are intravaginal.² Torsion is the most common pathology for males who undergo surgical exploration for scrotal pain.³

The main goal in the diagnosis and treatment of torsion is testicular salvage. Torsion is considered a urologic emergency, making early diagnosis and treatment critical to prevent testicular loss. In fact, a review of the relevant literature reveals that the rate of testicular salvage is much higher if the diagnosis is made within 6 to 12 hours.^1,2,5 Potential sequelae from delayed treatment include testicular infarction, loss of testicle, infertility problems, infections, cosmetic deformity, and increased risk for testicular malignancy.²

Because many men hesitate to seek medical attention for symptoms of testicular pain and swelling, the primary care clinician should openly discuss testicular disorders, especially with preadolescent males, during testicular examinations.⁶

Diagnosis

A testicular examination should be performed on any male presenting with a chief complaint of lower abdominal pain, back/flank pain, or any pain that radiates to the groin. The cremasteric reflex should be assessed because it can help differentiate among the causes of testicular pain.⁷ It is performed by gently stroking the upper inner thigh and observing for contraction of the ipsilateral testicle. One study found that, in cases of torsion, the absence of a cremasteric reflex had a sensitivity of 96% and a specificity of 88%.⁷ See the Table for the differential diagnosis for acute testicular pain.

While it is often possible to make the diagnosis of testicular torsion clinically, ultrasound with color Doppler is the diagnostic test of choice in cases for which the cause of acute scrotal pain is unclear.⁸ Ultrasound provides anatomic detail of the scrotum and its contents, and perfusion is assessed by adding the color Doppler images.⁸ It is important to note that, while the absence of blood flow is considered diagnostic for testicular torsion, the presence of flow does not necessarily exclude it.⁴

On the next page: Treatment >>

Treatment

Surgical exploration with intraoperative detorsion and orchiopexy (fixation of the testicle to the scrotal wall) is the mainstay of treatment for testicular torsion.¹ Orchiopexy is often performed bilaterally in order to prevent future torsion of the unaffected testicle. In about 40% of males with the bell clapper deformity, the condition is present on both sides.² Orchiectomy, the complete removal of the testicle, is necessary when the degree of torsion and subsequent ischemia have caused irreversible damage to the testicle.⁶ In one study in which 2,248 cases of torsion were reviewed, approximately 34% of males required orchiectomy.⁶

If surgery may be delayed, the clinician may attempt manual detorsion at the bedside. Despite the “open book” method described in many texts—which instructs the practitioner to rotate the testicle laterally—a review of the literature reveals that torsion takes place medially only 70% of the time.^1,5 The clinician should always consider this when any attempts at manual detorsion are made and correlate his or her technique with physical examination and the patient’s response.⁵

Relief of pain and return of the testicle to its natural longitudinal lie are considered indicators of successful detorsion.¹ Color Doppler ultrasound should be used to confirm the return of circulation. However, in one case review of pediatric patients who underwent surgical exploration after manual detorsion, some degree of residual torsion remained in 32%.⁵ Because of this risk, surgery is still indicated even in cases of successful bedside detorsion.⁵

On the next page: Case continuation >> 

CASE CONTINUATION

The decision to perform bedside ultrasound was made because the diagnosis of testicular torsion is a surgical emergency, and the window of time to prevent complications can be extremely narrow. If the ultrasound had been normal, then a CT scan may have provided additional data on which to base the diagnosis.

The patient was given adequate parenteral pain medication. After color Doppler ultrasound confirmed the torsion, the testicle was laterally rotated approximately 360°. The patient reported alleviation of his symptoms. Color Doppler was again performed to confirm the return of hyperemic blood flow to the affected testicle (Figure 2). The urologist arrived shortly thereafter and the patient was taken to the operating room, where he underwent scrotal exploration and bilateral orchiopexy.

On the next page: Conclusion >>

CONCLUSION

A testicular examination should be performed on any male presenting with a chief complaint of lower abdominal pain, back/flank pain, or any pain that radiates to the groin. Testicular torsion is most commonly seen in infants and adolescents but can occur at any age. The condition is a surgical emergency and the goal is testicular salvage, which is most likely to occur before 12 hours have elapsed since the onset of symptoms. An important component of the physical examination is attempting to elicit the cremasteric reflex, which is likely to be absent in the presence of torsion.

The primary care provider’s goal is to rapidly diagnose testicular torsion, then refer the patient immediately to a urologist or ED. The skilled clinician may attempt manual detorsion, based on his/her expertise and comfort level; however, this procedure should never delay prompt surgical intervention.

REFERENCES

1. Eyre RC. Evaluation of the acute scrotum in adults. www.uptodate.com/contents/evaluation-of-the-acute-scrotum-in-adults. Accessed May 16, 2014.

2. Ogunyemi OI, Weiker M, Abel EJ. Testicular torsion. http://emedicine.medscape.com/article/2036003-overview. Accessed May 16, 2014.

3. Khan F, Muoka O, Watson GM. Bell clapper testis, torsion, and detorsion: a case report. Case Rep Urol. 2011;2011:631970.

4. Molokwu CN, Somani BK, Goodman CM. Outcomes of scrotal exploration for acute scrotal pain suspicious of testicular torsion: a consecutive case series of 173 patients. BJU Int. 2011;107(6):990-993.

5. Sessions AE, Rabinowitz R, Hulbert WC, et al. Testicular torsion: direction, degree, duration and disinformation. J Urol. 2003;169(2):663-665.

6. Mansbach JM, Forbes P, Peters C. Testicular torsion and risk factors for orchiectomy. Arch Pediatr Adolesc Med. 2005;159:1167-1171.

7. Schmitz D, Safranek S. How useful is a physical exam in diagnosing testicular torsion? J Fam Pract. 2009;58(8):433-434.

8. D’Andrea A, Coppolino F, Cesarano E, et al. US in the assessment of acute scrotum. Crit Ultrasound J. 2013;5(suppl 1):S8. www.criticalultrasound journal.com/content/5/S1/S8/. Accessed May 16, 2014.

A 26-year-old man presented to the emergency department (ED) with a chief complaint of abdominal pain. After triage was complete, he was transported to an examination room, where the clinician obtained the history of presenting illness. The onset of pain was approximately 90 minutes prior to arrival at the ED and woke the patient from a “sound sleep.”  He stated that the pain initially started as a “3 out of 10” but had progressed to a “12 out of 10,” and he described it as being in the right lower quadrant of his abdomen, with radiation to his right testicle. However, he was unsure where the pain started or if it was worse in either location. Nausea was the primary associated symptom, but he denied vomiting, diarrhea, fever, dysuria, or hematuria. Last, the patient denied history of trauma.   

Medical history was noncontributory: He denied previous gastrointestinal diseases, and there was no history of renal stones, urinary tract infection, or any other genitourinary disease. He had no surgical history. The patient smoked less than a pack of cigarettes per day but denied alcohol or drug use.

Physical examination revealed a young man in moderate discomfort. Despite describing his pain as a “12 out of 10,” he had a blood pressure of 121/72 mm Hg; pulse, 59 beats/min; respiratory rate, 20 breaths/min; and temperature, 96.8°F. HEENT and cardiovascular, respiratory, musculoskeletal, and neurologic exam results were all within normal limits. Abdominal examination revealed a mildly tender right lower quadrant with deep palpation, but no rebound or guarding. Murphy sign was negative.

Because of the complaint of pain radiating to the testicles, a genitourinary examination was performed. The penis appeared unremarkable, with no lesions or discharge. There was no inguinal lymphadenopathy. The scrotum appeared appropriate in size and was also grossly unremarkable. The left testicle was nontender. However, palpation of the right testicle elicited moderate to severe pain. There was no visible swelling, and there were no palpable hernias or other masses. Cremasteric reflex was assessed bilaterally and deemed to be absent on the right side.

A workup was initiated that included a complete blood count, comprehensive metabolic panel, and urinalysis; the results of these tests were unremarkable. A differential diagnosis was formed, with emphasis on appendicitis and testicular torsion. Because of the specific nature and location of the pain, both ultrasound and CT of the abdomen/pelvis were considered. It was decided to order the ultrasound, with a plan to perform CT only if ultrasound was unremarkable. The patient was medicated for his pain and the ultrasound commenced. Halfway through the imaging, the clinician and attending physician were summoned to the examination room to review the image seen in Figure 1.

On the next page: Discussion and diagnosis >>

DISCUSSION

Testicular torsion may occur if the testicle twists or rotates on the spermatic cord. The twisting causes arterial ischemia and venous outflow obstruction, cutting off the testicle’s blood supply.^1,2 Torsion may be extravaginal or intravaginal, depending on the extent of involvement of the surrounding structures.²

Extravaginal torsion is most commonly seen in neonates and occurs because the entire testicle may freely rotate prior to fixation to the scrotal wall via the tunica vaginalis.²Intravaginal torsion is more common in adolescents and often occurs as a result of a condition known as bell clapper deformity. This congenital abnormality enables the testicle to rotate within the tunica vaginalis and rest transversely in the scrotum instead of in a more vertical orientation.^2,3 Torsion occurs if the testicle rotates 90° to 180°, with complete torsion occurring at 360° (torsion may extend to as much as 720°).² Torsion may also occur as a result of trauma.¹

Peak incidence of testicular torsion occurs at ages 13 to 14, but it can occur at any age; torsion affects approximately 1 in 4,000 males younger than 25.^2-5 Ninety-five percent of all torsions are intravaginal.² Torsion is the most common pathology for males who undergo surgical exploration for scrotal pain.³

The main goal in the diagnosis and treatment of torsion is testicular salvage. Torsion is considered a urologic emergency, making early diagnosis and treatment critical to prevent testicular loss. In fact, a review of the relevant literature reveals that the rate of testicular salvage is much higher if the diagnosis is made within 6 to 12 hours.^1,2,5 Potential sequelae from delayed treatment include testicular infarction, loss of testicle, infertility problems, infections, cosmetic deformity, and increased risk for testicular malignancy.²

Because many men hesitate to seek medical attention for symptoms of testicular pain and swelling, the primary care clinician should openly discuss testicular disorders, especially with preadolescent males, during testicular examinations.⁶

Diagnosis

A testicular examination should be performed on any male presenting with a chief complaint of lower abdominal pain, back/flank pain, or any pain that radiates to the groin. The cremasteric reflex should be assessed because it can help differentiate among the causes of testicular pain.⁷ It is performed by gently stroking the upper inner thigh and observing for contraction of the ipsilateral testicle. One study found that, in cases of torsion, the absence of a cremasteric reflex had a sensitivity of 96% and a specificity of 88%.⁷ See the Table for the differential diagnosis for acute testicular pain.

While it is often possible to make the diagnosis of testicular torsion clinically, ultrasound with color Doppler is the diagnostic test of choice in cases for which the cause of acute scrotal pain is unclear.⁸ Ultrasound provides anatomic detail of the scrotum and its contents, and perfusion is assessed by adding the color Doppler images.⁸ It is important to note that, while the absence of blood flow is considered diagnostic for testicular torsion, the presence of flow does not necessarily exclude it.⁴

On the next page: Treatment >>

Treatment

Surgical exploration with intraoperative detorsion and orchiopexy (fixation of the testicle to the scrotal wall) is the mainstay of treatment for testicular torsion.¹ Orchiopexy is often performed bilaterally in order to prevent future torsion of the unaffected testicle. In about 40% of males with the bell clapper deformity, the condition is present on both sides.² Orchiectomy, the complete removal of the testicle, is necessary when the degree of torsion and subsequent ischemia have caused irreversible damage to the testicle.⁶ In one study in which 2,248 cases of torsion were reviewed, approximately 34% of males required orchiectomy.⁶

If surgery may be delayed, the clinician may attempt manual detorsion at the bedside. Despite the “open book” method described in many texts—which instructs the practitioner to rotate the testicle laterally—a review of the literature reveals that torsion takes place medially only 70% of the time.^1,5 The clinician should always consider this when any attempts at manual detorsion are made and correlate his or her technique with physical examination and the patient’s response.⁵

Relief of pain and return of the testicle to its natural longitudinal lie are considered indicators of successful detorsion.¹ Color Doppler ultrasound should be used to confirm the return of circulation. However, in one case review of pediatric patients who underwent surgical exploration after manual detorsion, some degree of residual torsion remained in 32%.⁵ Because of this risk, surgery is still indicated even in cases of successful bedside detorsion.⁵

On the next page: Case continuation >> 

CASE CONTINUATION

The decision to perform bedside ultrasound was made because the diagnosis of testicular torsion is a surgical emergency, and the window of time to prevent complications can be extremely narrow. If the ultrasound had been normal, then a CT scan may have provided additional data on which to base the diagnosis.

The patient was given adequate parenteral pain medication. After color Doppler ultrasound confirmed the torsion, the testicle was laterally rotated approximately 360°. The patient reported alleviation of his symptoms. Color Doppler was again performed to confirm the return of hyperemic blood flow to the affected testicle (Figure 2). The urologist arrived shortly thereafter and the patient was taken to the operating room, where he underwent scrotal exploration and bilateral orchiopexy.

On the next page: Conclusion >>

CONCLUSION

A testicular examination should be performed on any male presenting with a chief complaint of lower abdominal pain, back/flank pain, or any pain that radiates to the groin. Testicular torsion is most commonly seen in infants and adolescents but can occur at any age. The condition is a surgical emergency and the goal is testicular salvage, which is most likely to occur before 12 hours have elapsed since the onset of symptoms. An important component of the physical examination is attempting to elicit the cremasteric reflex, which is likely to be absent in the presence of torsion.

The primary care provider’s goal is to rapidly diagnose testicular torsion, then refer the patient immediately to a urologist or ED. The skilled clinician may attempt manual detorsion, based on his/her expertise and comfort level; however, this procedure should never delay prompt surgical intervention.

REFERENCES

1. Eyre RC. Evaluation of the acute scrotum in adults. www.uptodate.com/contents/evaluation-of-the-acute-scrotum-in-adults. Accessed May 16, 2014.

2. Ogunyemi OI, Weiker M, Abel EJ. Testicular torsion. http://emedicine.medscape.com/article/2036003-overview. Accessed May 16, 2014.

3. Khan F, Muoka O, Watson GM. Bell clapper testis, torsion, and detorsion: a case report. Case Rep Urol. 2011;2011:631970.

4. Molokwu CN, Somani BK, Goodman CM. Outcomes of scrotal exploration for acute scrotal pain suspicious of testicular torsion: a consecutive case series of 173 patients. BJU Int. 2011;107(6):990-993.

5. Sessions AE, Rabinowitz R, Hulbert WC, et al. Testicular torsion: direction, degree, duration and disinformation. J Urol. 2003;169(2):663-665.

6. Mansbach JM, Forbes P, Peters C. Testicular torsion and risk factors for orchiectomy. Arch Pediatr Adolesc Med. 2005;159:1167-1171.

7. Schmitz D, Safranek S. How useful is a physical exam in diagnosing testicular torsion? J Fam Pract. 2009;58(8):433-434.

8. D’Andrea A, Coppolino F, Cesarano E, et al. US in the assessment of acute scrotum. Crit Ultrasound J. 2013;5(suppl 1):S8. www.criticalultrasound journal.com/content/5/S1/S8/. Accessed May 16, 2014.

A 20-year-old woman presents to the emergency department with fatigue and the sudden onset of palpitations. She reports no history of significant illness or surgery. She says she is not currently taking prescription or over-the-counter medications. She does not smoke, drink alcohol, or use illicit drugs.

Her weight is 52 kg (115 lb), her height is 170 cm (67 in), and her body mass index (BMI) is 18 kg/m². Vital signs: temperature 35.7°C (96.4°F), blood pressure 92/48 mm Hg, heart rate 73 bpm, respiratory rate 5 breaths per minute, and oxygen saturation 98% on room air.

She appears tired but is alert, conversant, and cooperative. Her skin is normal, and dentition is fair. Her pulse is regular, and respirations are slow. The abdomen is soft, non-tender, and flat. Strength is 4 on a scale of 5 in all extremities. Deep-tendon reflexes are 2+ and symmetric.

Electrocardiography (Figure 1) in the emergency department shows ST-segment depression, a prolonged corrected QT interval of 665 msec, T-wave inversion, PR prolongation, increased P-wave amplitude, and U waves.

1. Which electrolyte abnormality is associated with this electrocardiographic picture?

• Hypercalcemia
• Hyperkalemia
• Hypocalcemia
• Hypokalemia

Hypokalemia is the likely cause of these findings. The finding of U waves is considered significant when they are inverted, merged with the T wave, or have an amplitude greater than the T wave.¹ U waves are best seen in the precordial leads. When severe, hypokalemia can lead to potentially fatal arrhythmias such as high-grade atrioventricular block, ventricular tachycardia, and ventricular fibrillation.²

Hyperkalemia is associated with peaked T waves, a prolonged PR interval, decreased P wave amplitude, and a widened QRS complex.² When acute and severe, hyperkalemia is associated with ventricular arrhythmia.

Hypocalcemia is associated with a prolonged QT interval and ventricular dysrhythmia, but not U waves.²

Hypercalcemia is associated with bradydysrhythmia, as well as with a shortened QT interval.²

LABORATORY TESTING

Laboratory testing shows the following:

• Sodium 126 mmol/L (reference range 135–145)
• Potassium 1.5 mmol/L (3.5–5.1)
• Chloride 58 mmol/L (100–110)
• Bicarbonate 62 mmol/L (20–30)
• Blood urea nitrogen 16 mg/dL (7–18)
• Creatinine 0.8 mg/dL (0.5–1.0)
• Glucose 106 mg/dL (70–110)
• Ionized calcium 4.4 mg/dL (4.5–5.3)
• Magnesium 1.8 mg/dL (1.7–2.3)
• Phosphorus 4.1 mg/dL (2.5–4.5)
• Venous blood gases pH 7.56 (7.35–7.45), Pco₂ 69 mm Hg (35–45).

POTASSIUM HOMEOSTASIS

Ninety-eight percent of potassium is intracellular and only 2% is extracellular.³ The main cellular stores are myocytes and hepatocytes. Patients with decreased muscle mass may be at a higher risk of hypokalemia as a result of decreased skeletal muscle stores.⁴

The acute development of hypokalemia occurs from transcellular shifts. Alkalosis, insulin secretion, and beta-adrenergic stimulation promote the intracellular uptake of potassium. The major hormonal regulator of potassium excretion is aldosterone, which is stimulated by renal hypoperfusion and promotes potassium-ion secretion in the distal convoluted tubule.

Chronic hypokalemia develops in patients with ongoing renal or gastrointestinal potassium loss. If the cause of potassium loss is not elucidated by the history, the physical, and a review of medications, then one of two things is possible: either the patient has renal tubular disease affecting acid-base and potassium regulation, causing excessive mineralocorticoid secretion, which is associated with an abnormal response to aldosterone; or the patient is not being forthcoming in the history.

2. Which is the most likely cause of hypokalemia in this patient?

• Vomiting
• Liddle syndrome
• Bartter syndrome
• Gitelman syndrome
• Diuretic use

Her laboratory tests reveal hypokalemia and hyponatremic-hypochloremic metabolic alkalosis with compensatory respiratory acidosis. In metabolic alkalosis, the expected respiratory compensation is an increase of 0.7 mm Hg in Pco₂ for each 1-mEq/L increase in bicarbonate. Therefore, the expected Pco₂ is 67, close to the patient’s actual value of 69.

Protracted vomiting with loss of gastric acid juices could be a cause of the metabolic disturbances in this young woman, although she did not mention vomiting during the history.

Liddle syndrome, or pseudoaldosteronism, is a rare autosomal dominant disorder characterized by altered renal epithelial sodium channels, excessive sodium retention, and resultant hypertension. Hypokalemia and alkalosis are seen in Liddle syndrome, but the absence of hypertension in our patient makes Liddle syndrome unlikely.

Bartter syndrome is an inherited autosomal recessive disorder of the sodium-potassium-chloride cotransporter in the thick ascending loop of Henle, resulting in impaired reabsorption of chloride and sodium. Bartter syndrome mimics chronic loop-diuretic use and is associated with hypercalciuria. Bartter syndrome is possible in this patient; however, patients with Bartter syndrome are usually diagnosed in infancy or childhood and have evidence of growth impairment.

Gitelman syndrome is an autosomal recessive disorder of the thiazide-sensitive sodium-chloride cotransporter. Although Gitelman syndrome is more common than Bartter syndrome and presents at older ages, it is not usually associated with such profound metabolic alkalosis. Gitelman syndrome mimics chronic use of thiazide diuretics and is associated with hypocalciuria.

Diuretic use could also cause the metabolic disturbances described; however, the patient denied taking diuretics.

The most common cause of hypokalemia in clinical practice is diuretic use.⁴ In this young woman with unexplained hypokalemia, the most likely cause is either undisclosed self-induced vomiting or diuretic abuse. The degree of metabolic alkalosis suggests vomiting, since metabolic alkalosis this severe is usually seen only with protracted vomiting. Bartter and Gitelman syndromes are included in the differential diagnosis, but they are much less common than hypokalemia associated with diuretics or self-induced vomiting.⁵

3. Which test could help elucidate the cause of hypokalemia in this patient?

• Ratio of plasma aldosterone to rennin
• Urine chloride
• Ratio of urinary potassium to creatinine
• Urinary anion gap and urinary pH

APPROACH TO HYPOKALEMIA

Determining the cause of hypokalemia starts with a thorough history and physical examination. The history should focus on drugs such as diuretics and laxatives. Women should be asked about their menstrual history since irregular periods may suggest an eating disorder. The physical examination should focus on signs that suggest self-induced vomiting, such as dry skin, dental erosions, enlarged parotid glands, and calluses or scars on the knuckles.

Patients with an unclear cause of hypokalemia after a thorough history and physical examination can be categorized into one of three groups based on blood pressure and acid-base status:

• Hypokalemia, hypertension, metabolic alkalosis
• Hypokalemia, normal blood pressure, metabolic acidosis
• Hypokalemia, normal blood pressure, metabolic alkalosis.

Hypokalemia, hypertension, metabolic alkalosis

The blood pressure provides an important clue in the evaluation of hypokalemia. The combination of hypertension, hypokalemia, and alkalosis should raise concern for hyperaldosteronism or pseudoaldosteronism. Primary hyperaldosteronism from an adrenal adenoma (Conn syndrome) is characterized by a plasma aldosterone-renin ratio of greater than 20.^6,7 In contrast, patients with secondary hyperaldosteronism due to renovascular disease have a plasma aldosterone-renin ratio of less than 10. Patients with pseudoaldosteronism have low aldosterone and renin levels and hypertension. Since our patient has a normal blood pressure, testing the plasma aldosterone and renin levels would not help determine the cause of her hypokalemia.

Hypokalemia, normal blood pressure, metabolic acidosis

Patients with normal blood pressure, hypokalemia, and normal plasma anion gap acidosis either have renal tubular acidosis or have lost potassium because of diarrhea or laxative abuse. In a patient who denies taking laxatives or denies a history of diarrhea, checking the urinary anion gap and urinary pH may help differentiate the cause of acidosis and hypokalemia.

The urinary anion gap, calculated by the equation sodium + potassium − chloride, is an indirect estimate of hydrogen excretion in the form of ammonium ion⁸; the normal value is 0 to 10 mEq/L. A negative value represents increased hydrogen excretion in response to systemic acidosis from gastrointestinal or renal loss of bicarbonate (proximal renal tubular acidosis). A urinary pH greater than 5.5 in the setting of systemic acidosis suggests impaired ability of the kidneys to acidify urine and raises the possibility of renal tubular acidosis.

This patient has metabolic alkalosis, so calculation of the urinary anion gap would not be helpful.

Hypokalemia, normal blood pressure, metabolic alkalosis

Patients such as ours, with normal blood pressure, hypokalemia, and alkalosis, have been vomiting, have used diuretics, or have an inherited renal tubulopathy such as Bartter or Gitelman syndrome. Usually, differentiating Bartter and Gitelman syndromes from chronic vomiting or diuretic use is done with the history and physical examination. However, in patients with a questionable history and a lack of findings on physical examination, checking the urinary chloride, potassium, calcium, and creatinine may be helpful.

A urinary potassium-creatinine ratio greater than 15 suggests renal loss, whereas a ratio less than 15 suggests extrarenal loss.⁹

Patients who are taking a diuretic or who have Bartter or Gitelman syndrome have a high urinary chloride concentration, ie, greater than 20 mmol/L, whereas patients with hypokalemia and alkalosis from chronic vomiting tend to have a concentration less than 10 mmol/L.¹⁰

Table 1 summarizes an approach to the evaluation of unexplained hypokalemia based on blood pressure and acid-base status.

A HIDDEN HISTORY

On further questioning, the patient admits to an 8-year history of daily self-induced vomiting in an attempt to lose weight, in addition to multiple hospitalizations for hypokalemia and a previous diagnosis of an eating disorder.

INITIAL MANAGEMENT OF HYPOKALEMIA

The initial management of hypokalemia should focus on life-threatening emergencies. While patients with potassium levels greater than 3 mmol/L are usually asymptomatic, those with levels below 3 mmol/L present with muscle weakness and rhabdomyolysis.⁴ An acute drop in serum potassium to less than 2 mmol/L is associated with respiratory muscle weakness and ventricular arrhythmias.⁴ If the patient has cardiac symptoms or hypoventilation due to respiratory muscle weakness, continuous monitoring in the intensive care unit and aggressive therapy are warranted.

4. Which potassium formulation is most appropriate for the treatment of hypokalemia in this patient?

• Potassium chloride
• Potassium phosphate
• Potassium acetate

Oral potassium is preferable in patients with a serum potassium above 2.5 mmol/L.^4,11 Potassium phosphate should be used when supplementation with both potassium and phosphorus is needed. Potassium acetate should be reserved for patients with acidosis and hypokalemia. Otherwise, potassium chloride is typically preferred.^4,12 It comes in liquid and tablet forms. Liquid forms have an unpleasant taste, whereas tablets are usually well tolerated. No more than 20 to 40 mEq of potassium chloride tablets should be given at a time, since higher doses are associated with gastrointestinal mucosal injury.¹²

Potassium chloride is particularly preferred in patients with metabolic alkalosis, since increased chloride intake and delivery to the distal tubule increases the expression of pendrin, a luminal chloride and bicarbonate exchanger in the cortical collecting duct.¹³ With metabolic alkalosis, increased excretion of bicarbonate occurs through up-regulation of pendrin. Potassium depletion down-regulates pendrin.¹³ Additionally, correction of metabolic alkalosis increases serum potassium by movement of potassium from the intracellular to the extracellular space.

Intravenous potassium should be reserved for patients with severe hypokalemia (< 2.5 mmol/L) or significant arrhythmias.¹¹ Oral and intravenous potassium can safely be given simultaneously.¹¹ The intravenous rate should not exceed more than 10 to 20 mEq of potassium chloride per hour unless the patient has a life-threatening arrhythmia, respiratory failure, or severe hypokalemia.^14,15 In life-threatening situations, a femoral line should be placed, and potassium should be given as rapidly as 20 mEq over 15 to 20 minutes.¹⁴ Cannulation of the subclavian and internal jugular veins should be avoided in severe hypokalemia since mechanical irritation from guidewire placement can provoke ventricular arrhythmias.¹⁴

During intravenous administration of potassium, laboratory monitoring after every 20 mEq of potassium chloride is advised because of the possibility of rebound hyperkalemia. In patients with severe hypokalemia, avoidance of factors that can worsen intracellular shift of potassium is also important. Avoid dextrose-containing fluids to prevent insulin-induced shifting of potassium into cells. Restore intravascular volume to blunt hypovolemia-induced renin and aldosterone secretion. If a patient presents with severe hypokalemia and acidosis, correct the hypokalemia before the acidosis to avoid intracellular shift of potassium.

OUR PATIENT’S MANAGEMENT AND FOLLOW-UP PLAN

Given the severity of our patient’s hypokalemia and her complaint of palpitations, she was admitted to the hospital for monitoring. She required 180 mEq of intravenous potassium chloride and 140 mEq of oral potassium chloride during the first 24 hours in order to achieve a serum potassium level above 3 mmol/L. Electrocardiographic U waves resolved once the level was above 2 mmol/L, and ST depressions resolved once it was above 3 mmol/L. The QT interval normalized after 24 hours of hospitalization.

On discharge, she was prescribed oral potassium chloride 40 mEq daily and magnesium sulfate 400 mg twice daily, with plans for a followup visit with her outpatient therapy team, which includes a psychiatrist, a social worker, and her primary care provider. She declined a referral for inpatient therapy but agreed to a goal of decreasing the frequency of induced vomiting and outpatient visits. She was also educated on how and when to access emergency medical care.¹⁶

A 20-year-old woman presents to the emergency department with fatigue and the sudden onset of palpitations. She reports no history of significant illness or surgery. She says she is not currently taking prescription or over-the-counter medications. She does not smoke, drink alcohol, or use illicit drugs.

Her weight is 52 kg (115 lb), her height is 170 cm (67 in), and her body mass index (BMI) is 18 kg/m². Vital signs: temperature 35.7°C (96.4°F), blood pressure 92/48 mm Hg, heart rate 73 bpm, respiratory rate 5 breaths per minute, and oxygen saturation 98% on room air.

She appears tired but is alert, conversant, and cooperative. Her skin is normal, and dentition is fair. Her pulse is regular, and respirations are slow. The abdomen is soft, non-tender, and flat. Strength is 4 on a scale of 5 in all extremities. Deep-tendon reflexes are 2+ and symmetric.

Electrocardiography (Figure 1) in the emergency department shows ST-segment depression, a prolonged corrected QT interval of 665 msec, T-wave inversion, PR prolongation, increased P-wave amplitude, and U waves.

1. Which electrolyte abnormality is associated with this electrocardiographic picture?

• Hypercalcemia
• Hyperkalemia
• Hypocalcemia
• Hypokalemia

Hypokalemia is the likely cause of these findings. The finding of U waves is considered significant when they are inverted, merged with the T wave, or have an amplitude greater than the T wave.¹ U waves are best seen in the precordial leads. When severe, hypokalemia can lead to potentially fatal arrhythmias such as high-grade atrioventricular block, ventricular tachycardia, and ventricular fibrillation.²

Hyperkalemia is associated with peaked T waves, a prolonged PR interval, decreased P wave amplitude, and a widened QRS complex.² When acute and severe, hyperkalemia is associated with ventricular arrhythmia.

Hypocalcemia is associated with a prolonged QT interval and ventricular dysrhythmia, but not U waves.²

Hypercalcemia is associated with bradydysrhythmia, as well as with a shortened QT interval.²

LABORATORY TESTING

Laboratory testing shows the following:

• Sodium 126 mmol/L (reference range 135–145)
• Potassium 1.5 mmol/L (3.5–5.1)
• Chloride 58 mmol/L (100–110)
• Bicarbonate 62 mmol/L (20–30)
• Blood urea nitrogen 16 mg/dL (7–18)
• Creatinine 0.8 mg/dL (0.5–1.0)
• Glucose 106 mg/dL (70–110)
• Ionized calcium 4.4 mg/dL (4.5–5.3)
• Magnesium 1.8 mg/dL (1.7–2.3)
• Phosphorus 4.1 mg/dL (2.5–4.5)
• Venous blood gases pH 7.56 (7.35–7.45), Pco₂ 69 mm Hg (35–45).

POTASSIUM HOMEOSTASIS

Ninety-eight percent of potassium is intracellular and only 2% is extracellular.³ The main cellular stores are myocytes and hepatocytes. Patients with decreased muscle mass may be at a higher risk of hypokalemia as a result of decreased skeletal muscle stores.⁴

The acute development of hypokalemia occurs from transcellular shifts. Alkalosis, insulin secretion, and beta-adrenergic stimulation promote the intracellular uptake of potassium. The major hormonal regulator of potassium excretion is aldosterone, which is stimulated by renal hypoperfusion and promotes potassium-ion secretion in the distal convoluted tubule.

Chronic hypokalemia develops in patients with ongoing renal or gastrointestinal potassium loss. If the cause of potassium loss is not elucidated by the history, the physical, and a review of medications, then one of two things is possible: either the patient has renal tubular disease affecting acid-base and potassium regulation, causing excessive mineralocorticoid secretion, which is associated with an abnormal response to aldosterone; or the patient is not being forthcoming in the history.

2. Which is the most likely cause of hypokalemia in this patient?

• Vomiting
• Liddle syndrome
• Bartter syndrome
• Gitelman syndrome
• Diuretic use

Her laboratory tests reveal hypokalemia and hyponatremic-hypochloremic metabolic alkalosis with compensatory respiratory acidosis. In metabolic alkalosis, the expected respiratory compensation is an increase of 0.7 mm Hg in Pco₂ for each 1-mEq/L increase in bicarbonate. Therefore, the expected Pco₂ is 67, close to the patient’s actual value of 69.

Protracted vomiting with loss of gastric acid juices could be a cause of the metabolic disturbances in this young woman, although she did not mention vomiting during the history.

Liddle syndrome, or pseudoaldosteronism, is a rare autosomal dominant disorder characterized by altered renal epithelial sodium channels, excessive sodium retention, and resultant hypertension. Hypokalemia and alkalosis are seen in Liddle syndrome, but the absence of hypertension in our patient makes Liddle syndrome unlikely.

Bartter syndrome is an inherited autosomal recessive disorder of the sodium-potassium-chloride cotransporter in the thick ascending loop of Henle, resulting in impaired reabsorption of chloride and sodium. Bartter syndrome mimics chronic loop-diuretic use and is associated with hypercalciuria. Bartter syndrome is possible in this patient; however, patients with Bartter syndrome are usually diagnosed in infancy or childhood and have evidence of growth impairment.

Gitelman syndrome is an autosomal recessive disorder of the thiazide-sensitive sodium-chloride cotransporter. Although Gitelman syndrome is more common than Bartter syndrome and presents at older ages, it is not usually associated with such profound metabolic alkalosis. Gitelman syndrome mimics chronic use of thiazide diuretics and is associated with hypocalciuria.

Diuretic use could also cause the metabolic disturbances described; however, the patient denied taking diuretics.

The most common cause of hypokalemia in clinical practice is diuretic use.⁴ In this young woman with unexplained hypokalemia, the most likely cause is either undisclosed self-induced vomiting or diuretic abuse. The degree of metabolic alkalosis suggests vomiting, since metabolic alkalosis this severe is usually seen only with protracted vomiting. Bartter and Gitelman syndromes are included in the differential diagnosis, but they are much less common than hypokalemia associated with diuretics or self-induced vomiting.⁵

3. Which test could help elucidate the cause of hypokalemia in this patient?

• Ratio of plasma aldosterone to rennin
• Urine chloride
• Ratio of urinary potassium to creatinine
• Urinary anion gap and urinary pH

APPROACH TO HYPOKALEMIA

Determining the cause of hypokalemia starts with a thorough history and physical examination. The history should focus on drugs such as diuretics and laxatives. Women should be asked about their menstrual history since irregular periods may suggest an eating disorder. The physical examination should focus on signs that suggest self-induced vomiting, such as dry skin, dental erosions, enlarged parotid glands, and calluses or scars on the knuckles.

Patients with an unclear cause of hypokalemia after a thorough history and physical examination can be categorized into one of three groups based on blood pressure and acid-base status:

• Hypokalemia, hypertension, metabolic alkalosis
• Hypokalemia, normal blood pressure, metabolic acidosis
• Hypokalemia, normal blood pressure, metabolic alkalosis.

Hypokalemia, hypertension, metabolic alkalosis

The blood pressure provides an important clue in the evaluation of hypokalemia. The combination of hypertension, hypokalemia, and alkalosis should raise concern for hyperaldosteronism or pseudoaldosteronism. Primary hyperaldosteronism from an adrenal adenoma (Conn syndrome) is characterized by a plasma aldosterone-renin ratio of greater than 20.^6,7 In contrast, patients with secondary hyperaldosteronism due to renovascular disease have a plasma aldosterone-renin ratio of less than 10. Patients with pseudoaldosteronism have low aldosterone and renin levels and hypertension. Since our patient has a normal blood pressure, testing the plasma aldosterone and renin levels would not help determine the cause of her hypokalemia.

Hypokalemia, normal blood pressure, metabolic acidosis

Patients with normal blood pressure, hypokalemia, and normal plasma anion gap acidosis either have renal tubular acidosis or have lost potassium because of diarrhea or laxative abuse. In a patient who denies taking laxatives or denies a history of diarrhea, checking the urinary anion gap and urinary pH may help differentiate the cause of acidosis and hypokalemia.

The urinary anion gap, calculated by the equation sodium + potassium − chloride, is an indirect estimate of hydrogen excretion in the form of ammonium ion⁸; the normal value is 0 to 10 mEq/L. A negative value represents increased hydrogen excretion in response to systemic acidosis from gastrointestinal or renal loss of bicarbonate (proximal renal tubular acidosis). A urinary pH greater than 5.5 in the setting of systemic acidosis suggests impaired ability of the kidneys to acidify urine and raises the possibility of renal tubular acidosis.

This patient has metabolic alkalosis, so calculation of the urinary anion gap would not be helpful.

Hypokalemia, normal blood pressure, metabolic alkalosis

Patients such as ours, with normal blood pressure, hypokalemia, and alkalosis, have been vomiting, have used diuretics, or have an inherited renal tubulopathy such as Bartter or Gitelman syndrome. Usually, differentiating Bartter and Gitelman syndromes from chronic vomiting or diuretic use is done with the history and physical examination. However, in patients with a questionable history and a lack of findings on physical examination, checking the urinary chloride, potassium, calcium, and creatinine may be helpful.

A urinary potassium-creatinine ratio greater than 15 suggests renal loss, whereas a ratio less than 15 suggests extrarenal loss.⁹

Patients who are taking a diuretic or who have Bartter or Gitelman syndrome have a high urinary chloride concentration, ie, greater than 20 mmol/L, whereas patients with hypokalemia and alkalosis from chronic vomiting tend to have a concentration less than 10 mmol/L.¹⁰

Table 1 summarizes an approach to the evaluation of unexplained hypokalemia based on blood pressure and acid-base status.

A HIDDEN HISTORY

On further questioning, the patient admits to an 8-year history of daily self-induced vomiting in an attempt to lose weight, in addition to multiple hospitalizations for hypokalemia and a previous diagnosis of an eating disorder.

INITIAL MANAGEMENT OF HYPOKALEMIA

The initial management of hypokalemia should focus on life-threatening emergencies. While patients with potassium levels greater than 3 mmol/L are usually asymptomatic, those with levels below 3 mmol/L present with muscle weakness and rhabdomyolysis.⁴ An acute drop in serum potassium to less than 2 mmol/L is associated with respiratory muscle weakness and ventricular arrhythmias.⁴ If the patient has cardiac symptoms or hypoventilation due to respiratory muscle weakness, continuous monitoring in the intensive care unit and aggressive therapy are warranted.

4. Which potassium formulation is most appropriate for the treatment of hypokalemia in this patient?

• Potassium chloride
• Potassium phosphate
• Potassium acetate

Oral potassium is preferable in patients with a serum potassium above 2.5 mmol/L.^4,11 Potassium phosphate should be used when supplementation with both potassium and phosphorus is needed. Potassium acetate should be reserved for patients with acidosis and hypokalemia. Otherwise, potassium chloride is typically preferred.^4,12 It comes in liquid and tablet forms. Liquid forms have an unpleasant taste, whereas tablets are usually well tolerated. No more than 20 to 40 mEq of potassium chloride tablets should be given at a time, since higher doses are associated with gastrointestinal mucosal injury.¹²

Potassium chloride is particularly preferred in patients with metabolic alkalosis, since increased chloride intake and delivery to the distal tubule increases the expression of pendrin, a luminal chloride and bicarbonate exchanger in the cortical collecting duct.¹³ With metabolic alkalosis, increased excretion of bicarbonate occurs through up-regulation of pendrin. Potassium depletion down-regulates pendrin.¹³ Additionally, correction of metabolic alkalosis increases serum potassium by movement of potassium from the intracellular to the extracellular space.

Intravenous potassium should be reserved for patients with severe hypokalemia (< 2.5 mmol/L) or significant arrhythmias.¹¹ Oral and intravenous potassium can safely be given simultaneously.¹¹ The intravenous rate should not exceed more than 10 to 20 mEq of potassium chloride per hour unless the patient has a life-threatening arrhythmia, respiratory failure, or severe hypokalemia.^14,15 In life-threatening situations, a femoral line should be placed, and potassium should be given as rapidly as 20 mEq over 15 to 20 minutes.¹⁴ Cannulation of the subclavian and internal jugular veins should be avoided in severe hypokalemia since mechanical irritation from guidewire placement can provoke ventricular arrhythmias.¹⁴

During intravenous administration of potassium, laboratory monitoring after every 20 mEq of potassium chloride is advised because of the possibility of rebound hyperkalemia. In patients with severe hypokalemia, avoidance of factors that can worsen intracellular shift of potassium is also important. Avoid dextrose-containing fluids to prevent insulin-induced shifting of potassium into cells. Restore intravascular volume to blunt hypovolemia-induced renin and aldosterone secretion. If a patient presents with severe hypokalemia and acidosis, correct the hypokalemia before the acidosis to avoid intracellular shift of potassium.

OUR PATIENT’S MANAGEMENT AND FOLLOW-UP PLAN

Given the severity of our patient’s hypokalemia and her complaint of palpitations, she was admitted to the hospital for monitoring. She required 180 mEq of intravenous potassium chloride and 140 mEq of oral potassium chloride during the first 24 hours in order to achieve a serum potassium level above 3 mmol/L. Electrocardiographic U waves resolved once the level was above 2 mmol/L, and ST depressions resolved once it was above 3 mmol/L. The QT interval normalized after 24 hours of hospitalization.

On discharge, she was prescribed oral potassium chloride 40 mEq daily and magnesium sulfate 400 mg twice daily, with plans for a followup visit with her outpatient therapy team, which includes a psychiatrist, a social worker, and her primary care provider. She declined a referral for inpatient therapy but agreed to a goal of decreasing the frequency of induced vomiting and outpatient visits. She was also educated on how and when to access emergency medical care.¹⁶

A 20-year-old woman presents to the emergency department with fatigue and the sudden onset of palpitations. She reports no history of significant illness or surgery. She says she is not currently taking prescription or over-the-counter medications. She does not smoke, drink alcohol, or use illicit drugs.

Her weight is 52 kg (115 lb), her height is 170 cm (67 in), and her body mass index (BMI) is 18 kg/m². Vital signs: temperature 35.7°C (96.4°F), blood pressure 92/48 mm Hg, heart rate 73 bpm, respiratory rate 5 breaths per minute, and oxygen saturation 98% on room air.

She appears tired but is alert, conversant, and cooperative. Her skin is normal, and dentition is fair. Her pulse is regular, and respirations are slow. The abdomen is soft, non-tender, and flat. Strength is 4 on a scale of 5 in all extremities. Deep-tendon reflexes are 2+ and symmetric.

Electrocardiography (Figure 1) in the emergency department shows ST-segment depression, a prolonged corrected QT interval of 665 msec, T-wave inversion, PR prolongation, increased P-wave amplitude, and U waves.

1. Which electrolyte abnormality is associated with this electrocardiographic picture?

• Hypercalcemia
• Hyperkalemia
• Hypocalcemia
• Hypokalemia

Hypokalemia is the likely cause of these findings. The finding of U waves is considered significant when they are inverted, merged with the T wave, or have an amplitude greater than the T wave.¹ U waves are best seen in the precordial leads. When severe, hypokalemia can lead to potentially fatal arrhythmias such as high-grade atrioventricular block, ventricular tachycardia, and ventricular fibrillation.²

Hyperkalemia is associated with peaked T waves, a prolonged PR interval, decreased P wave amplitude, and a widened QRS complex.² When acute and severe, hyperkalemia is associated with ventricular arrhythmia.

Hypocalcemia is associated with a prolonged QT interval and ventricular dysrhythmia, but not U waves.²

Hypercalcemia is associated with bradydysrhythmia, as well as with a shortened QT interval.²

LABORATORY TESTING

Laboratory testing shows the following:

• Sodium 126 mmol/L (reference range 135–145)
• Potassium 1.5 mmol/L (3.5–5.1)
• Chloride 58 mmol/L (100–110)
• Bicarbonate 62 mmol/L (20–30)
• Blood urea nitrogen 16 mg/dL (7–18)
• Creatinine 0.8 mg/dL (0.5–1.0)
• Glucose 106 mg/dL (70–110)
• Ionized calcium 4.4 mg/dL (4.5–5.3)
• Magnesium 1.8 mg/dL (1.7–2.3)
• Phosphorus 4.1 mg/dL (2.5–4.5)
• Venous blood gases pH 7.56 (7.35–7.45), Pco₂ 69 mm Hg (35–45).

POTASSIUM HOMEOSTASIS

Ninety-eight percent of potassium is intracellular and only 2% is extracellular.³ The main cellular stores are myocytes and hepatocytes. Patients with decreased muscle mass may be at a higher risk of hypokalemia as a result of decreased skeletal muscle stores.⁴

The acute development of hypokalemia occurs from transcellular shifts. Alkalosis, insulin secretion, and beta-adrenergic stimulation promote the intracellular uptake of potassium. The major hormonal regulator of potassium excretion is aldosterone, which is stimulated by renal hypoperfusion and promotes potassium-ion secretion in the distal convoluted tubule.

Chronic hypokalemia develops in patients with ongoing renal or gastrointestinal potassium loss. If the cause of potassium loss is not elucidated by the history, the physical, and a review of medications, then one of two things is possible: either the patient has renal tubular disease affecting acid-base and potassium regulation, causing excessive mineralocorticoid secretion, which is associated with an abnormal response to aldosterone; or the patient is not being forthcoming in the history.

2. Which is the most likely cause of hypokalemia in this patient?

• Vomiting
• Liddle syndrome
• Bartter syndrome
• Gitelman syndrome
• Diuretic use

Her laboratory tests reveal hypokalemia and hyponatremic-hypochloremic metabolic alkalosis with compensatory respiratory acidosis. In metabolic alkalosis, the expected respiratory compensation is an increase of 0.7 mm Hg in Pco₂ for each 1-mEq/L increase in bicarbonate. Therefore, the expected Pco₂ is 67, close to the patient’s actual value of 69.

Protracted vomiting with loss of gastric acid juices could be a cause of the metabolic disturbances in this young woman, although she did not mention vomiting during the history.

Liddle syndrome, or pseudoaldosteronism, is a rare autosomal dominant disorder characterized by altered renal epithelial sodium channels, excessive sodium retention, and resultant hypertension. Hypokalemia and alkalosis are seen in Liddle syndrome, but the absence of hypertension in our patient makes Liddle syndrome unlikely.

Bartter syndrome is an inherited autosomal recessive disorder of the sodium-potassium-chloride cotransporter in the thick ascending loop of Henle, resulting in impaired reabsorption of chloride and sodium. Bartter syndrome mimics chronic loop-diuretic use and is associated with hypercalciuria. Bartter syndrome is possible in this patient; however, patients with Bartter syndrome are usually diagnosed in infancy or childhood and have evidence of growth impairment.

Gitelman syndrome is an autosomal recessive disorder of the thiazide-sensitive sodium-chloride cotransporter. Although Gitelman syndrome is more common than Bartter syndrome and presents at older ages, it is not usually associated with such profound metabolic alkalosis. Gitelman syndrome mimics chronic use of thiazide diuretics and is associated with hypocalciuria.

Diuretic use could also cause the metabolic disturbances described; however, the patient denied taking diuretics.

The most common cause of hypokalemia in clinical practice is diuretic use.⁴ In this young woman with unexplained hypokalemia, the most likely cause is either undisclosed self-induced vomiting or diuretic abuse. The degree of metabolic alkalosis suggests vomiting, since metabolic alkalosis this severe is usually seen only with protracted vomiting. Bartter and Gitelman syndromes are included in the differential diagnosis, but they are much less common than hypokalemia associated with diuretics or self-induced vomiting.⁵

3. Which test could help elucidate the cause of hypokalemia in this patient?

• Ratio of plasma aldosterone to rennin
• Urine chloride
• Ratio of urinary potassium to creatinine
• Urinary anion gap and urinary pH

APPROACH TO HYPOKALEMIA

Determining the cause of hypokalemia starts with a thorough history and physical examination. The history should focus on drugs such as diuretics and laxatives. Women should be asked about their menstrual history since irregular periods may suggest an eating disorder. The physical examination should focus on signs that suggest self-induced vomiting, such as dry skin, dental erosions, enlarged parotid glands, and calluses or scars on the knuckles.

Patients with an unclear cause of hypokalemia after a thorough history and physical examination can be categorized into one of three groups based on blood pressure and acid-base status:

• Hypokalemia, hypertension, metabolic alkalosis
• Hypokalemia, normal blood pressure, metabolic acidosis
• Hypokalemia, normal blood pressure, metabolic alkalosis.

Hypokalemia, hypertension, metabolic alkalosis

The blood pressure provides an important clue in the evaluation of hypokalemia. The combination of hypertension, hypokalemia, and alkalosis should raise concern for hyperaldosteronism or pseudoaldosteronism. Primary hyperaldosteronism from an adrenal adenoma (Conn syndrome) is characterized by a plasma aldosterone-renin ratio of greater than 20.^6,7 In contrast, patients with secondary hyperaldosteronism due to renovascular disease have a plasma aldosterone-renin ratio of less than 10. Patients with pseudoaldosteronism have low aldosterone and renin levels and hypertension. Since our patient has a normal blood pressure, testing the plasma aldosterone and renin levels would not help determine the cause of her hypokalemia.

Hypokalemia, normal blood pressure, metabolic acidosis

Patients with normal blood pressure, hypokalemia, and normal plasma anion gap acidosis either have renal tubular acidosis or have lost potassium because of diarrhea or laxative abuse. In a patient who denies taking laxatives or denies a history of diarrhea, checking the urinary anion gap and urinary pH may help differentiate the cause of acidosis and hypokalemia.

The urinary anion gap, calculated by the equation sodium + potassium − chloride, is an indirect estimate of hydrogen excretion in the form of ammonium ion⁸; the normal value is 0 to 10 mEq/L. A negative value represents increased hydrogen excretion in response to systemic acidosis from gastrointestinal or renal loss of bicarbonate (proximal renal tubular acidosis). A urinary pH greater than 5.5 in the setting of systemic acidosis suggests impaired ability of the kidneys to acidify urine and raises the possibility of renal tubular acidosis.

This patient has metabolic alkalosis, so calculation of the urinary anion gap would not be helpful.

Hypokalemia, normal blood pressure, metabolic alkalosis

Patients such as ours, with normal blood pressure, hypokalemia, and alkalosis, have been vomiting, have used diuretics, or have an inherited renal tubulopathy such as Bartter or Gitelman syndrome. Usually, differentiating Bartter and Gitelman syndromes from chronic vomiting or diuretic use is done with the history and physical examination. However, in patients with a questionable history and a lack of findings on physical examination, checking the urinary chloride, potassium, calcium, and creatinine may be helpful.

A urinary potassium-creatinine ratio greater than 15 suggests renal loss, whereas a ratio less than 15 suggests extrarenal loss.⁹

Patients who are taking a diuretic or who have Bartter or Gitelman syndrome have a high urinary chloride concentration, ie, greater than 20 mmol/L, whereas patients with hypokalemia and alkalosis from chronic vomiting tend to have a concentration less than 10 mmol/L.¹⁰

Table 1 summarizes an approach to the evaluation of unexplained hypokalemia based on blood pressure and acid-base status.

A HIDDEN HISTORY

On further questioning, the patient admits to an 8-year history of daily self-induced vomiting in an attempt to lose weight, in addition to multiple hospitalizations for hypokalemia and a previous diagnosis of an eating disorder.

INITIAL MANAGEMENT OF HYPOKALEMIA

The initial management of hypokalemia should focus on life-threatening emergencies. While patients with potassium levels greater than 3 mmol/L are usually asymptomatic, those with levels below 3 mmol/L present with muscle weakness and rhabdomyolysis.⁴ An acute drop in serum potassium to less than 2 mmol/L is associated with respiratory muscle weakness and ventricular arrhythmias.⁴ If the patient has cardiac symptoms or hypoventilation due to respiratory muscle weakness, continuous monitoring in the intensive care unit and aggressive therapy are warranted.

4. Which potassium formulation is most appropriate for the treatment of hypokalemia in this patient?

• Potassium chloride
• Potassium phosphate
• Potassium acetate

Oral potassium is preferable in patients with a serum potassium above 2.5 mmol/L.^4,11 Potassium phosphate should be used when supplementation with both potassium and phosphorus is needed. Potassium acetate should be reserved for patients with acidosis and hypokalemia. Otherwise, potassium chloride is typically preferred.^4,12 It comes in liquid and tablet forms. Liquid forms have an unpleasant taste, whereas tablets are usually well tolerated. No more than 20 to 40 mEq of potassium chloride tablets should be given at a time, since higher doses are associated with gastrointestinal mucosal injury.¹²

Potassium chloride is particularly preferred in patients with metabolic alkalosis, since increased chloride intake and delivery to the distal tubule increases the expression of pendrin, a luminal chloride and bicarbonate exchanger in the cortical collecting duct.¹³ With metabolic alkalosis, increased excretion of bicarbonate occurs through up-regulation of pendrin. Potassium depletion down-regulates pendrin.¹³ Additionally, correction of metabolic alkalosis increases serum potassium by movement of potassium from the intracellular to the extracellular space.

Intravenous potassium should be reserved for patients with severe hypokalemia (< 2.5 mmol/L) or significant arrhythmias.¹¹ Oral and intravenous potassium can safely be given simultaneously.¹¹ The intravenous rate should not exceed more than 10 to 20 mEq of potassium chloride per hour unless the patient has a life-threatening arrhythmia, respiratory failure, or severe hypokalemia.^14,15 In life-threatening situations, a femoral line should be placed, and potassium should be given as rapidly as 20 mEq over 15 to 20 minutes.¹⁴ Cannulation of the subclavian and internal jugular veins should be avoided in severe hypokalemia since mechanical irritation from guidewire placement can provoke ventricular arrhythmias.¹⁴

During intravenous administration of potassium, laboratory monitoring after every 20 mEq of potassium chloride is advised because of the possibility of rebound hyperkalemia. In patients with severe hypokalemia, avoidance of factors that can worsen intracellular shift of potassium is also important. Avoid dextrose-containing fluids to prevent insulin-induced shifting of potassium into cells. Restore intravascular volume to blunt hypovolemia-induced renin and aldosterone secretion. If a patient presents with severe hypokalemia and acidosis, correct the hypokalemia before the acidosis to avoid intracellular shift of potassium.

OUR PATIENT’S MANAGEMENT AND FOLLOW-UP PLAN

Given the severity of our patient’s hypokalemia and her complaint of palpitations, she was admitted to the hospital for monitoring. She required 180 mEq of intravenous potassium chloride and 140 mEq of oral potassium chloride during the first 24 hours in order to achieve a serum potassium level above 3 mmol/L. Electrocardiographic U waves resolved once the level was above 2 mmol/L, and ST depressions resolved once it was above 3 mmol/L. The QT interval normalized after 24 hours of hospitalization.

On discharge, she was prescribed oral potassium chloride 40 mEq daily and magnesium sulfate 400 mg twice daily, with plans for a followup visit with her outpatient therapy team, which includes a psychiatrist, a social worker, and her primary care provider. She declined a referral for inpatient therapy but agreed to a goal of decreasing the frequency of induced vomiting and outpatient visits. She was also educated on how and when to access emergency medical care.¹⁶

ANSWER

The radiograph demonstrates no acute osseous injury, such as fracture or dislocation. Of interest and note is increased sclerosis within both femoral heads, more so on the left versus the right side. Given the patient’s young age, such findings could be related to early avascular necrosis. His clinical symptoms certainly correlate. MRI or bone scan, as well as orthopedic evaluation, is warranted in such a case. 

Fortunately, subsequent MRI of both hips did not show any avascular necrosis but rather osteoarthritic changes. The MRI of his spinal column was negative as well.

ANSWER

The radiograph demonstrates no acute osseous injury, such as fracture or dislocation. Of interest and note is increased sclerosis within both femoral heads, more so on the left versus the right side. Given the patient’s young age, such findings could be related to early avascular necrosis. His clinical symptoms certainly correlate. MRI or bone scan, as well as orthopedic evaluation, is warranted in such a case. 

Fortunately, subsequent MRI of both hips did not show any avascular necrosis but rather osteoarthritic changes. The MRI of his spinal column was negative as well.

ANSWER

The radiograph demonstrates no acute osseous injury, such as fracture or dislocation. Of interest and note is increased sclerosis within both femoral heads, more so on the left versus the right side. Given the patient’s young age, such findings could be related to early avascular necrosis. His clinical symptoms certainly correlate. MRI or bone scan, as well as orthopedic evaluation, is warranted in such a case. 

Fortunately, subsequent MRI of both hips did not show any avascular necrosis but rather osteoarthritic changes. The MRI of his spinal column was negative as well.