Case Reports

The connection between idiopathic thrombocytopenic purpura (ITP) and Grave's disease is not well known in the Western hemisphere. The immunologic relationship between these 2 conditions is well reported15 but poorly defined in the literature. New‐onset hyperthyroidism in the setting of preexisting ITP can be overlooked and, if untreated, lead to worsening of the ITP, rendering it refractory to standard therapy. Early recognition and treatment of the hyperthyroid state with antithyroid medications can lead to significant improvement in the platelet count.1, 8 We report this rare but critical clinical relationship.

CASE REPORT

A 35‐year‐old Asian woman with a known history of stable ITP for 12 years (baseline platelet count of 40,000/mL) presented to her outpatient provider with a diffuse petechial rash, easy bruisability, and heavy menorrhagia for 2 weeks. Her new platelet count was 7000/mL. She was immediately started on prednisone at a dose of 1 mg/kg without any improvement in her platelet count. At the end of 4 weeks on prednisone, she developed fever, intractable nausea and vomiting, severe headache, hypotension, and tachycardia. She was subsequently hospitalized with the presumptive diagnosis of meningitis and sepsis syndrome. Her clinical syndrome was consistent with systemic inflammatory response syndrome. She was treated aggressively with intravenous fluids and a broad‐spectrum empirical antimicrobial regimen consisting of ceftriaxone, vancomycin, and acyclovir. Lumbar puncture was deferred because of her low platelet count. The sepsis workup, which included viral, fungal, and bacterial blood cultures, remained negative. Her peripheral smear did not show evidence of microangiopathic hemolytic anemia, therefore ruling out thrombotic thrombocytopenic purpura and disseminated intravascular coagulation. HIV and tuberculosis were also ruled out. After the initial sepsis workup turned out negative, she was started on solumedrol 125 mg IV every 6 hours. Over the next 2 weeks, she received an average of 4‐6 units of platelets per day and multiple blood transfusions to maintain her hemoglobin and platelet counts. The latter remained in the 1000‐5000 platelets/mL range throughout her hospitalization without any significant improvement. Her clinical course was further complicated by multiple small intracranial hemorrhages without major focal neurological deficits. A bone marrow biopsy was eventually done. It showed early dysplastic cells but no definite features of myelodysplasia and few large megakaryocytes. She received 1 dose of vincristine without response in the bone marrow after 2 weeks, and consideration was given to treatment with rituximab for refractory ITP. At that point, she informed her hematologist that 10 years ago, she had been treated for hyperthyroidism with antithyroid medications for 6 months, without further follow‐up. A thyroid panel was then ordered, and she was found to be hyperthyroid, with thyroid‐stimulating hormone (TSH) 0.01 mU/mL and free T4 of 3.1 ng/dL. She was subsequently started on propylthiouracil at 300 mg per day. Her platelet count dramatically improved and went up to the 50,000/mm³ range without further intervention over the next few months. After her discharge, an outpatient thyroid scan showed diffuse, homogeneous uptake of iodine, thereby confirming the diagnosis of Grave's disease. Retrospectively, her initial clinical syndrome of fever, hypotension, and tachycardia may have been the result of thyrotoxicosis or worsened by it.

DISCUSSION

The association between ITP and Grave's disease is poorly understood. Many hypotheses from observational data have been given in the literature. The leading theory to explain the coexistence of these 2 disorders is the presence of a common autoimmune pathway with production of 2 kinds of antibodies against platelets and TSH receptors. Indeed, autoimmune disorders tend to occur concurrently in individuals or families. Bizzaro et al. reported the coexistence of ITP and Grave's in 4 members of the same family.6 Hymes et al. found elevated levels of platelet‐bound IgG in 44% of 25 study patients with Grave's thyrotoxicosis.7 Most of these patients had easy bruising and/or bleeding, and 12% were thrombocytopenic. Panzer et al. reported the presence of antiplatelet IgG in patients with Grave's as well as improved platelet counts and increased mean platelet volume after successful antithyroid therapy.8

In addition to the coexistence of thyroid‐stimulatingimmunoglobulins (TSIs) and antiplatelet antibodies as a potential mechanism for Grave's‐associated thrombocytopenia, some have postulated that in Grave's patients, TSIs and other thyroid antibodies might actually bind to the platelets themselves. The postulated site for binding would be a truncated actin‐binding protein on the platelets that would link the high‐affinity Fc receptor of immunoglobulin G to the platelets' cytoskeleton, thereby accelerating their destruction.9

Another plausible mechanism is activation of the reticuloendothelial system by thyroid hormones, with increased clearance of platelets by the spleen in thyrotoxic states. This may explain the restoration of the platelet count when euthyroidism is reached.

Finally, thyrotoxicosis seems to alter platelet aggregation, partially by inhibition of myosin light‐chain kinase, and that also improves with restoration of euthyroidism.10

The coexistence of severe hyperthyroidism and thrombocytopenia can mimic severe sepsis in critically ill patients, and the hyperthyroid state in itself can worsen the thrombocytopenia of ITP. We suspect this patient's severe sepsis may actually have been an unrecognized severe thyrotoxicosis, with bone marrow dysfunction secondary to the hyperthyroidism, which might partially explain her lack of response to standard therapy.

CONCLUSIONS

This case underscores the importance of screening for and treating hyperthyroidism in patients with ITP, especially those resistant to steroid therapy, because the literature seems to indicate that treatment of the hyperthyroid state improves platelet count. This might help to prevent devastating clinical complications. Further research is necessary to define this empirical finding.

The connection between idiopathic thrombocytopenic purpura (ITP) and Grave's disease is not well known in the Western hemisphere. The immunologic relationship between these 2 conditions is well reported15 but poorly defined in the literature. New‐onset hyperthyroidism in the setting of preexisting ITP can be overlooked and, if untreated, lead to worsening of the ITP, rendering it refractory to standard therapy. Early recognition and treatment of the hyperthyroid state with antithyroid medications can lead to significant improvement in the platelet count.1, 8 We report this rare but critical clinical relationship.

CASE REPORT

A 35‐year‐old Asian woman with a known history of stable ITP for 12 years (baseline platelet count of 40,000/mL) presented to her outpatient provider with a diffuse petechial rash, easy bruisability, and heavy menorrhagia for 2 weeks. Her new platelet count was 7000/mL. She was immediately started on prednisone at a dose of 1 mg/kg without any improvement in her platelet count. At the end of 4 weeks on prednisone, she developed fever, intractable nausea and vomiting, severe headache, hypotension, and tachycardia. She was subsequently hospitalized with the presumptive diagnosis of meningitis and sepsis syndrome. Her clinical syndrome was consistent with systemic inflammatory response syndrome. She was treated aggressively with intravenous fluids and a broad‐spectrum empirical antimicrobial regimen consisting of ceftriaxone, vancomycin, and acyclovir. Lumbar puncture was deferred because of her low platelet count. The sepsis workup, which included viral, fungal, and bacterial blood cultures, remained negative. Her peripheral smear did not show evidence of microangiopathic hemolytic anemia, therefore ruling out thrombotic thrombocytopenic purpura and disseminated intravascular coagulation. HIV and tuberculosis were also ruled out. After the initial sepsis workup turned out negative, she was started on solumedrol 125 mg IV every 6 hours. Over the next 2 weeks, she received an average of 4‐6 units of platelets per day and multiple blood transfusions to maintain her hemoglobin and platelet counts. The latter remained in the 1000‐5000 platelets/mL range throughout her hospitalization without any significant improvement. Her clinical course was further complicated by multiple small intracranial hemorrhages without major focal neurological deficits. A bone marrow biopsy was eventually done. It showed early dysplastic cells but no definite features of myelodysplasia and few large megakaryocytes. She received 1 dose of vincristine without response in the bone marrow after 2 weeks, and consideration was given to treatment with rituximab for refractory ITP. At that point, she informed her hematologist that 10 years ago, she had been treated for hyperthyroidism with antithyroid medications for 6 months, without further follow‐up. A thyroid panel was then ordered, and she was found to be hyperthyroid, with thyroid‐stimulating hormone (TSH) 0.01 mU/mL and free T4 of 3.1 ng/dL. She was subsequently started on propylthiouracil at 300 mg per day. Her platelet count dramatically improved and went up to the 50,000/mm³ range without further intervention over the next few months. After her discharge, an outpatient thyroid scan showed diffuse, homogeneous uptake of iodine, thereby confirming the diagnosis of Grave's disease. Retrospectively, her initial clinical syndrome of fever, hypotension, and tachycardia may have been the result of thyrotoxicosis or worsened by it.

DISCUSSION

The association between ITP and Grave's disease is poorly understood. Many hypotheses from observational data have been given in the literature. The leading theory to explain the coexistence of these 2 disorders is the presence of a common autoimmune pathway with production of 2 kinds of antibodies against platelets and TSH receptors. Indeed, autoimmune disorders tend to occur concurrently in individuals or families. Bizzaro et al. reported the coexistence of ITP and Grave's in 4 members of the same family.6 Hymes et al. found elevated levels of platelet‐bound IgG in 44% of 25 study patients with Grave's thyrotoxicosis.7 Most of these patients had easy bruising and/or bleeding, and 12% were thrombocytopenic. Panzer et al. reported the presence of antiplatelet IgG in patients with Grave's as well as improved platelet counts and increased mean platelet volume after successful antithyroid therapy.8

In addition to the coexistence of thyroid‐stimulatingimmunoglobulins (TSIs) and antiplatelet antibodies as a potential mechanism for Grave's‐associated thrombocytopenia, some have postulated that in Grave's patients, TSIs and other thyroid antibodies might actually bind to the platelets themselves. The postulated site for binding would be a truncated actin‐binding protein on the platelets that would link the high‐affinity Fc receptor of immunoglobulin G to the platelets' cytoskeleton, thereby accelerating their destruction.9

Another plausible mechanism is activation of the reticuloendothelial system by thyroid hormones, with increased clearance of platelets by the spleen in thyrotoxic states. This may explain the restoration of the platelet count when euthyroidism is reached.

Finally, thyrotoxicosis seems to alter platelet aggregation, partially by inhibition of myosin light‐chain kinase, and that also improves with restoration of euthyroidism.10

The coexistence of severe hyperthyroidism and thrombocytopenia can mimic severe sepsis in critically ill patients, and the hyperthyroid state in itself can worsen the thrombocytopenia of ITP. We suspect this patient's severe sepsis may actually have been an unrecognized severe thyrotoxicosis, with bone marrow dysfunction secondary to the hyperthyroidism, which might partially explain her lack of response to standard therapy.

CONCLUSIONS

This case underscores the importance of screening for and treating hyperthyroidism in patients with ITP, especially those resistant to steroid therapy, because the literature seems to indicate that treatment of the hyperthyroid state improves platelet count. This might help to prevent devastating clinical complications. Further research is necessary to define this empirical finding.

The connection between idiopathic thrombocytopenic purpura (ITP) and Grave's disease is not well known in the Western hemisphere. The immunologic relationship between these 2 conditions is well reported15 but poorly defined in the literature. New‐onset hyperthyroidism in the setting of preexisting ITP can be overlooked and, if untreated, lead to worsening of the ITP, rendering it refractory to standard therapy. Early recognition and treatment of the hyperthyroid state with antithyroid medications can lead to significant improvement in the platelet count.1, 8 We report this rare but critical clinical relationship.

CASE REPORT

A 35‐year‐old Asian woman with a known history of stable ITP for 12 years (baseline platelet count of 40,000/mL) presented to her outpatient provider with a diffuse petechial rash, easy bruisability, and heavy menorrhagia for 2 weeks. Her new platelet count was 7000/mL. She was immediately started on prednisone at a dose of 1 mg/kg without any improvement in her platelet count. At the end of 4 weeks on prednisone, she developed fever, intractable nausea and vomiting, severe headache, hypotension, and tachycardia. She was subsequently hospitalized with the presumptive diagnosis of meningitis and sepsis syndrome. Her clinical syndrome was consistent with systemic inflammatory response syndrome. She was treated aggressively with intravenous fluids and a broad‐spectrum empirical antimicrobial regimen consisting of ceftriaxone, vancomycin, and acyclovir. Lumbar puncture was deferred because of her low platelet count. The sepsis workup, which included viral, fungal, and bacterial blood cultures, remained negative. Her peripheral smear did not show evidence of microangiopathic hemolytic anemia, therefore ruling out thrombotic thrombocytopenic purpura and disseminated intravascular coagulation. HIV and tuberculosis were also ruled out. After the initial sepsis workup turned out negative, she was started on solumedrol 125 mg IV every 6 hours. Over the next 2 weeks, she received an average of 4‐6 units of platelets per day and multiple blood transfusions to maintain her hemoglobin and platelet counts. The latter remained in the 1000‐5000 platelets/mL range throughout her hospitalization without any significant improvement. Her clinical course was further complicated by multiple small intracranial hemorrhages without major focal neurological deficits. A bone marrow biopsy was eventually done. It showed early dysplastic cells but no definite features of myelodysplasia and few large megakaryocytes. She received 1 dose of vincristine without response in the bone marrow after 2 weeks, and consideration was given to treatment with rituximab for refractory ITP. At that point, she informed her hematologist that 10 years ago, she had been treated for hyperthyroidism with antithyroid medications for 6 months, without further follow‐up. A thyroid panel was then ordered, and she was found to be hyperthyroid, with thyroid‐stimulating hormone (TSH) 0.01 mU/mL and free T4 of 3.1 ng/dL. She was subsequently started on propylthiouracil at 300 mg per day. Her platelet count dramatically improved and went up to the 50,000/mm³ range without further intervention over the next few months. After her discharge, an outpatient thyroid scan showed diffuse, homogeneous uptake of iodine, thereby confirming the diagnosis of Grave's disease. Retrospectively, her initial clinical syndrome of fever, hypotension, and tachycardia may have been the result of thyrotoxicosis or worsened by it.

DISCUSSION

The association between ITP and Grave's disease is poorly understood. Many hypotheses from observational data have been given in the literature. The leading theory to explain the coexistence of these 2 disorders is the presence of a common autoimmune pathway with production of 2 kinds of antibodies against platelets and TSH receptors. Indeed, autoimmune disorders tend to occur concurrently in individuals or families. Bizzaro et al. reported the coexistence of ITP and Grave's in 4 members of the same family.6 Hymes et al. found elevated levels of platelet‐bound IgG in 44% of 25 study patients with Grave's thyrotoxicosis.7 Most of these patients had easy bruising and/or bleeding, and 12% were thrombocytopenic. Panzer et al. reported the presence of antiplatelet IgG in patients with Grave's as well as improved platelet counts and increased mean platelet volume after successful antithyroid therapy.8

In addition to the coexistence of thyroid‐stimulatingimmunoglobulins (TSIs) and antiplatelet antibodies as a potential mechanism for Grave's‐associated thrombocytopenia, some have postulated that in Grave's patients, TSIs and other thyroid antibodies might actually bind to the platelets themselves. The postulated site for binding would be a truncated actin‐binding protein on the platelets that would link the high‐affinity Fc receptor of immunoglobulin G to the platelets' cytoskeleton, thereby accelerating their destruction.9

Another plausible mechanism is activation of the reticuloendothelial system by thyroid hormones, with increased clearance of platelets by the spleen in thyrotoxic states. This may explain the restoration of the platelet count when euthyroidism is reached.

Finally, thyrotoxicosis seems to alter platelet aggregation, partially by inhibition of myosin light‐chain kinase, and that also improves with restoration of euthyroidism.10

The coexistence of severe hyperthyroidism and thrombocytopenia can mimic severe sepsis in critically ill patients, and the hyperthyroid state in itself can worsen the thrombocytopenia of ITP. We suspect this patient's severe sepsis may actually have been an unrecognized severe thyrotoxicosis, with bone marrow dysfunction secondary to the hyperthyroidism, which might partially explain her lack of response to standard therapy.

CONCLUSIONS

This case underscores the importance of screening for and treating hyperthyroidism in patients with ITP, especially those resistant to steroid therapy, because the literature seems to indicate that treatment of the hyperthyroid state improves platelet count. This might help to prevent devastating clinical complications. Further research is necessary to define this empirical finding.

The patient is an 86‐year‐old woman with a history of mild dementia, major depression with psychotic features, congestive heart failure, hypertension, hyperlipidemia, osteoporosis, and hypothyroidism. She presented to her primary care physician (PCP) complaining of 4 days of bilateral lower extremity edema and dyspnea on exertion. She was admitted to the hospitalist service for exacerbation of congestive heart failure.

MEDICATIONS

Donepezil, olanzapine, mirtazapine, sertraline, spironolactone, triamterene/hydrochlorothizide, simvastatin, alendronate, levothyroxine, multivitamin.

SOCIAL HISTORY

She lived alone in an independent‐living retirement apartment that provided meals but not medical care, and she was able to function independently in her activities of daily living. Her pharmacy delivered her medications via courier service, whereas visiting home nurses filled her medication box and checked on her status weekly.

HOSPITAL COURSE

Admission vitals were: heart rate, 83; blood pressure, 158/84; respiratory rate, 20; temperature, 36.4, and saturation, 95% on room air. Echocardiogram revealed intact ejection fraction, left ventricular hypertrophy, and impaired relaxation. A TSH of 6.6 demonstrated undertreated hypothyroidism. Telemetry monitoring was significant for frequent short bursts of narrow‐complex tachycardia without clear atrial activity. The etiology of her heart failure exacerbation was presumed to be paroxysmal atrial fibrillation in the setting of diastolic dysfunction. Given her mild hyperkalemia (5.1), her diuretics were changed to monotherapy with furosemide. Low‐dose beta blockade and antithrombotic therapy were started as well as increased supplementation of levothyroxine. After several days of diuresis, her potassium had normalized, she tolerated initiation of a new ACE inhibitor, and her dyspnea had resolved. On the last hospital day, her dentures were accidentally discarded with her breakfast tray, causing her great distress.

On discharge she was on 4 new medications, 2 old medications had been stopped, and 1 prior medication's dose had been increased. During medication reconciliation, the patient reported that she had not been taking olanzapine for weeks, and thus this was omitted from her home health medication orders, with instructions to discuss with her PCP on first follow‐up within the week. The patient was provided with congestive heart failure instructions and a complete medication list. Unfortunately, the day of discharge was the first day of a holiday weekend.

Case management was unavailable on the weekend; her out‐of‐state family member was unable to be reached by phone, and her usual pharmacy courier service was closed. As she did not have a friend or family member to pick up her prescriptions from an alternate pharmacy, her prescriptions were provided as handwritten scripts, called in to her pharmacy's voice mail, and written on the home health orders. The patient was discharged to her home with communication to her PCP via telephone, e‐mail, and electronic discharge summary.

POSTDISCHARGE

Medications were not delivered to the patient until the third postdischarge day. Three days after discharge, the daughter from out of state left a message for the PCP expressing concern that the patient was failingnot eating or taking any of her medications. An expedited home nursing visit was arranged. Five days after discharge, the pharmacist called the PCP stating he had not received a prescription for the beta‐blocker. Her PCP saw the patient in clinic 6 days after discharge and reconciled the medication list, restarting the olanzapine that the patient had stopped a few weeks before and the mirtazapine, which had not been restarted despite its presence on the discharge orders and patient instructions. She continued to have poor appetite and mood and was taking her medications only with great effort from her visiting nurse and staff at the retirement community. A major cause of this decline was the significant worsening of her depression brought on by hospitalization, lapses in her psychiatric medications, and emotional distress induced by the loss of her dentures during her hospital stay. She was readmitted 10 days after her discharge because she was unable to care for herself.

DISCUSSION

This case demonstrates numerous pitfalls in the transition process. Despite communication between the hospitalists and the PCP and a common electronic medical record, this patient failed the transition from the acute care hospital to the ambulatory setting. On the holiday weekend, ancillary support services were unavailable, including case management to contact her home care agency and her pharmacy to fill and deliver her new prescriptions. Despite efforts by the discharging physician, the out‐of‐town family could not be contacted. Thus, an elderly woman with cognitive impairment was left to process a new diagnosis and 7 medication changes with an unreliable mechanism to obtain her new medications.

With the rise of hospital medicine, it has increasingly been recognized that transitions represent a point of vulnerability in the care of geriatric patients. A change in physical location of care and handoffs between caregivers create the potential for error and loss of information. Prior research has demonstrated frequent quantitative and qualitative deficiencies in the information conveyed between inpatient and outpatient physicians, with direct communication occurring less than 20% of the time.1 In this case, communication occurred between the hospitalists and the outpatient physician, demonstrating that communication is just one element of successful transitions.

Components of effective care transitions have been described in the literature, including: preparation of the patient and caregiver for the transition, medication reconciliation, instructions to patient and caregiver about symptoms and signs of worsening, and an explicit follow‐up plan for tests and appointments.2 Optimally, there is interactive discussion between the hospitalist and the receiving clinician with a summary of events including an updated medication, allergy, and problem list, current advance directives, and a common plan of care.2 This case illustrates that these elements are necessary but may not be sufficient.

Some interventions have been found to be effective. A nurse‐led multidisciplinary approach to the discharge of elderly patients with congestive heart failure led to decreased readmission rates after 90 days and was found to be a cost‐saving measure.3 Similar results have been seen in geriatric patients with a variety of diagnoses in trials using advanced‐practice nurses to bridge the vulnerable period of discharge or by interventions to improve the ability of family caregivers to handle the challenges of the transition.46 Individualized attention to the unique needs of each patient and members of their social support structure, and investment in resources to do so, has the ability to decrease readmissions.

Medication errors, medication omissions, or the inability to fill medications on discharge represent a patient safety challenge. There has been increasing emphasis on medication reconciliation at admission and discharge, but in some cases the gold standard medication list is hard to determine. Electronic medical records would seem to be a natural solution to this problem, but as this case illustrates, the electronic record may not reflect the reality of patient adherence. As in this case, clarification may require another visit with the primary provider, leaving a period of time with an uncertain medication list and therefore a vulnerable patient. Access to medications after discharge was also a problem in this case, but this is not rare. A 2001 study found that 2 days after discharge from a general medicine hospital service, 1 in 5 patients had been unable to obtain all discharge medications.7 A pharmacist‐led medication reconciliation intervention in nursing home patients led to decreases in length of stay and discrepancy‐related adverse drug events. Furthermore, a follow‐up call allowed for clarification of medication questions in 25% of cases.7, 8

Patient characteristics such as depression and cognitive dysfunction have been found to affect readmission rates and are important to assess in addressing risk for poor outcomes after discharge. A 2000 study comparing readmission rates after discharge from a geriatric rehabilitation hospital found that patients with depression had an odds ratio of 3.5 for readmission compared with those without depression.9 Inadequate health literacy is also associated with decreased ability to self‐manage chronic disease and is associated with increased risk of mortality in community‐dwelling elderly such as the patient in this case.10 Asking patients or their proxies to explain their own understanding of the discharge plan can unmask comprehension issues that otherwise may go undetected.

Discharge on a weekend presents a period of critical vulnerability. Early recognition that a transition is susceptible to failure allows the events necessary for success to occur during the week when services are available. An example in the present case might include having had the pharmacy fill the prescriptions prior to the day of discharge. This does introduce a new opportunity for error in cases in which the plan of care changes but would have solved the inability to have prescriptions filled once the holiday weekend had begun.

In cases in which the usual mechanisms break down, increased effort on the part of the hospitalist can usually create a unique solution to the problem. Examples of creative solutions that did not occur in this case might include contacting the manager of the patient's retirement apartment to determine if this individual might be willing to fill prescriptions at an alternate pharmacy. A better alternative would be to change the system such that the solution is readily accessible and time efficient. Weekend availability of case management would be one such step. A means for the hospital's inpatient pharmacy to provide 2‐3 days of bridging medications would prevent weekend prescription access from affecting timely discharges of multiple patients over the course of a year. The hospitalist is in a unique position to take a leadership role in effecting system change to address these issues.

Ultimately, it is the duty of the hospitalist to take responsibility for the safety and well‐being of the patient, and if no solution can be found, it may be necessary to hold discharge or find an alternate disposition until logistical hurdles have been overcome. Indeed, for patients admitted for myocardial infarction, discharges were less likely to occur on weekends, presumably because of lack of ancillary services.11 With foresight, creative problem solving, and systems improvement, this should rarely be necessary.

Transitions continue to be a difficult time for the most vulnerable patients. Intense efforts have improved outcomes in selected populations but have not been broadly applied. Identification of patients at the highest risk, such as those with depression, poor social support, and cognitive limitations, would allow anticipation of difficult transitions and potential utilization of proven interventions, such as advanced‐practice nurses or follow‐up pharmacy contact. Processes such as these might have prevented some of the problems in this patient's discharge. Appreciation of the weekend discharge as a time of particular challenges allows barriers to be identified and solutions created during the week, when resources are still available. Attention to all elements of effective transitions should become part of the growing culture of patient safety.

The patient is an 86‐year‐old woman with a history of mild dementia, major depression with psychotic features, congestive heart failure, hypertension, hyperlipidemia, osteoporosis, and hypothyroidism. She presented to her primary care physician (PCP) complaining of 4 days of bilateral lower extremity edema and dyspnea on exertion. She was admitted to the hospitalist service for exacerbation of congestive heart failure.

MEDICATIONS

Donepezil, olanzapine, mirtazapine, sertraline, spironolactone, triamterene/hydrochlorothizide, simvastatin, alendronate, levothyroxine, multivitamin.

SOCIAL HISTORY

She lived alone in an independent‐living retirement apartment that provided meals but not medical care, and she was able to function independently in her activities of daily living. Her pharmacy delivered her medications via courier service, whereas visiting home nurses filled her medication box and checked on her status weekly.

HOSPITAL COURSE

Admission vitals were: heart rate, 83; blood pressure, 158/84; respiratory rate, 20; temperature, 36.4, and saturation, 95% on room air. Echocardiogram revealed intact ejection fraction, left ventricular hypertrophy, and impaired relaxation. A TSH of 6.6 demonstrated undertreated hypothyroidism. Telemetry monitoring was significant for frequent short bursts of narrow‐complex tachycardia without clear atrial activity. The etiology of her heart failure exacerbation was presumed to be paroxysmal atrial fibrillation in the setting of diastolic dysfunction. Given her mild hyperkalemia (5.1), her diuretics were changed to monotherapy with furosemide. Low‐dose beta blockade and antithrombotic therapy were started as well as increased supplementation of levothyroxine. After several days of diuresis, her potassium had normalized, she tolerated initiation of a new ACE inhibitor, and her dyspnea had resolved. On the last hospital day, her dentures were accidentally discarded with her breakfast tray, causing her great distress.

On discharge she was on 4 new medications, 2 old medications had been stopped, and 1 prior medication's dose had been increased. During medication reconciliation, the patient reported that she had not been taking olanzapine for weeks, and thus this was omitted from her home health medication orders, with instructions to discuss with her PCP on first follow‐up within the week. The patient was provided with congestive heart failure instructions and a complete medication list. Unfortunately, the day of discharge was the first day of a holiday weekend.

Case management was unavailable on the weekend; her out‐of‐state family member was unable to be reached by phone, and her usual pharmacy courier service was closed. As she did not have a friend or family member to pick up her prescriptions from an alternate pharmacy, her prescriptions were provided as handwritten scripts, called in to her pharmacy's voice mail, and written on the home health orders. The patient was discharged to her home with communication to her PCP via telephone, e‐mail, and electronic discharge summary.

POSTDISCHARGE

Medications were not delivered to the patient until the third postdischarge day. Three days after discharge, the daughter from out of state left a message for the PCP expressing concern that the patient was failingnot eating or taking any of her medications. An expedited home nursing visit was arranged. Five days after discharge, the pharmacist called the PCP stating he had not received a prescription for the beta‐blocker. Her PCP saw the patient in clinic 6 days after discharge and reconciled the medication list, restarting the olanzapine that the patient had stopped a few weeks before and the mirtazapine, which had not been restarted despite its presence on the discharge orders and patient instructions. She continued to have poor appetite and mood and was taking her medications only with great effort from her visiting nurse and staff at the retirement community. A major cause of this decline was the significant worsening of her depression brought on by hospitalization, lapses in her psychiatric medications, and emotional distress induced by the loss of her dentures during her hospital stay. She was readmitted 10 days after her discharge because she was unable to care for herself.

DISCUSSION

This case demonstrates numerous pitfalls in the transition process. Despite communication between the hospitalists and the PCP and a common electronic medical record, this patient failed the transition from the acute care hospital to the ambulatory setting. On the holiday weekend, ancillary support services were unavailable, including case management to contact her home care agency and her pharmacy to fill and deliver her new prescriptions. Despite efforts by the discharging physician, the out‐of‐town family could not be contacted. Thus, an elderly woman with cognitive impairment was left to process a new diagnosis and 7 medication changes with an unreliable mechanism to obtain her new medications.

With the rise of hospital medicine, it has increasingly been recognized that transitions represent a point of vulnerability in the care of geriatric patients. A change in physical location of care and handoffs between caregivers create the potential for error and loss of information. Prior research has demonstrated frequent quantitative and qualitative deficiencies in the information conveyed between inpatient and outpatient physicians, with direct communication occurring less than 20% of the time.1 In this case, communication occurred between the hospitalists and the outpatient physician, demonstrating that communication is just one element of successful transitions.

Components of effective care transitions have been described in the literature, including: preparation of the patient and caregiver for the transition, medication reconciliation, instructions to patient and caregiver about symptoms and signs of worsening, and an explicit follow‐up plan for tests and appointments.2 Optimally, there is interactive discussion between the hospitalist and the receiving clinician with a summary of events including an updated medication, allergy, and problem list, current advance directives, and a common plan of care.2 This case illustrates that these elements are necessary but may not be sufficient.

Some interventions have been found to be effective. A nurse‐led multidisciplinary approach to the discharge of elderly patients with congestive heart failure led to decreased readmission rates after 90 days and was found to be a cost‐saving measure.3 Similar results have been seen in geriatric patients with a variety of diagnoses in trials using advanced‐practice nurses to bridge the vulnerable period of discharge or by interventions to improve the ability of family caregivers to handle the challenges of the transition.46 Individualized attention to the unique needs of each patient and members of their social support structure, and investment in resources to do so, has the ability to decrease readmissions.

Medication errors, medication omissions, or the inability to fill medications on discharge represent a patient safety challenge. There has been increasing emphasis on medication reconciliation at admission and discharge, but in some cases the gold standard medication list is hard to determine. Electronic medical records would seem to be a natural solution to this problem, but as this case illustrates, the electronic record may not reflect the reality of patient adherence. As in this case, clarification may require another visit with the primary provider, leaving a period of time with an uncertain medication list and therefore a vulnerable patient. Access to medications after discharge was also a problem in this case, but this is not rare. A 2001 study found that 2 days after discharge from a general medicine hospital service, 1 in 5 patients had been unable to obtain all discharge medications.7 A pharmacist‐led medication reconciliation intervention in nursing home patients led to decreases in length of stay and discrepancy‐related adverse drug events. Furthermore, a follow‐up call allowed for clarification of medication questions in 25% of cases.7, 8

Patient characteristics such as depression and cognitive dysfunction have been found to affect readmission rates and are important to assess in addressing risk for poor outcomes after discharge. A 2000 study comparing readmission rates after discharge from a geriatric rehabilitation hospital found that patients with depression had an odds ratio of 3.5 for readmission compared with those without depression.9 Inadequate health literacy is also associated with decreased ability to self‐manage chronic disease and is associated with increased risk of mortality in community‐dwelling elderly such as the patient in this case.10 Asking patients or their proxies to explain their own understanding of the discharge plan can unmask comprehension issues that otherwise may go undetected.

Discharge on a weekend presents a period of critical vulnerability. Early recognition that a transition is susceptible to failure allows the events necessary for success to occur during the week when services are available. An example in the present case might include having had the pharmacy fill the prescriptions prior to the day of discharge. This does introduce a new opportunity for error in cases in which the plan of care changes but would have solved the inability to have prescriptions filled once the holiday weekend had begun.

In cases in which the usual mechanisms break down, increased effort on the part of the hospitalist can usually create a unique solution to the problem. Examples of creative solutions that did not occur in this case might include contacting the manager of the patient's retirement apartment to determine if this individual might be willing to fill prescriptions at an alternate pharmacy. A better alternative would be to change the system such that the solution is readily accessible and time efficient. Weekend availability of case management would be one such step. A means for the hospital's inpatient pharmacy to provide 2‐3 days of bridging medications would prevent weekend prescription access from affecting timely discharges of multiple patients over the course of a year. The hospitalist is in a unique position to take a leadership role in effecting system change to address these issues.

Ultimately, it is the duty of the hospitalist to take responsibility for the safety and well‐being of the patient, and if no solution can be found, it may be necessary to hold discharge or find an alternate disposition until logistical hurdles have been overcome. Indeed, for patients admitted for myocardial infarction, discharges were less likely to occur on weekends, presumably because of lack of ancillary services.11 With foresight, creative problem solving, and systems improvement, this should rarely be necessary.

Transitions continue to be a difficult time for the most vulnerable patients. Intense efforts have improved outcomes in selected populations but have not been broadly applied. Identification of patients at the highest risk, such as those with depression, poor social support, and cognitive limitations, would allow anticipation of difficult transitions and potential utilization of proven interventions, such as advanced‐practice nurses or follow‐up pharmacy contact. Processes such as these might have prevented some of the problems in this patient's discharge. Appreciation of the weekend discharge as a time of particular challenges allows barriers to be identified and solutions created during the week, when resources are still available. Attention to all elements of effective transitions should become part of the growing culture of patient safety.

The patient is an 86‐year‐old woman with a history of mild dementia, major depression with psychotic features, congestive heart failure, hypertension, hyperlipidemia, osteoporosis, and hypothyroidism. She presented to her primary care physician (PCP) complaining of 4 days of bilateral lower extremity edema and dyspnea on exertion. She was admitted to the hospitalist service for exacerbation of congestive heart failure.

MEDICATIONS

Donepezil, olanzapine, mirtazapine, sertraline, spironolactone, triamterene/hydrochlorothizide, simvastatin, alendronate, levothyroxine, multivitamin.

SOCIAL HISTORY

She lived alone in an independent‐living retirement apartment that provided meals but not medical care, and she was able to function independently in her activities of daily living. Her pharmacy delivered her medications via courier service, whereas visiting home nurses filled her medication box and checked on her status weekly.

HOSPITAL COURSE

Admission vitals were: heart rate, 83; blood pressure, 158/84; respiratory rate, 20; temperature, 36.4, and saturation, 95% on room air. Echocardiogram revealed intact ejection fraction, left ventricular hypertrophy, and impaired relaxation. A TSH of 6.6 demonstrated undertreated hypothyroidism. Telemetry monitoring was significant for frequent short bursts of narrow‐complex tachycardia without clear atrial activity. The etiology of her heart failure exacerbation was presumed to be paroxysmal atrial fibrillation in the setting of diastolic dysfunction. Given her mild hyperkalemia (5.1), her diuretics were changed to monotherapy with furosemide. Low‐dose beta blockade and antithrombotic therapy were started as well as increased supplementation of levothyroxine. After several days of diuresis, her potassium had normalized, she tolerated initiation of a new ACE inhibitor, and her dyspnea had resolved. On the last hospital day, her dentures were accidentally discarded with her breakfast tray, causing her great distress.

On discharge she was on 4 new medications, 2 old medications had been stopped, and 1 prior medication's dose had been increased. During medication reconciliation, the patient reported that she had not been taking olanzapine for weeks, and thus this was omitted from her home health medication orders, with instructions to discuss with her PCP on first follow‐up within the week. The patient was provided with congestive heart failure instructions and a complete medication list. Unfortunately, the day of discharge was the first day of a holiday weekend.

Case management was unavailable on the weekend; her out‐of‐state family member was unable to be reached by phone, and her usual pharmacy courier service was closed. As she did not have a friend or family member to pick up her prescriptions from an alternate pharmacy, her prescriptions were provided as handwritten scripts, called in to her pharmacy's voice mail, and written on the home health orders. The patient was discharged to her home with communication to her PCP via telephone, e‐mail, and electronic discharge summary.

POSTDISCHARGE

Medications were not delivered to the patient until the third postdischarge day. Three days after discharge, the daughter from out of state left a message for the PCP expressing concern that the patient was failingnot eating or taking any of her medications. An expedited home nursing visit was arranged. Five days after discharge, the pharmacist called the PCP stating he had not received a prescription for the beta‐blocker. Her PCP saw the patient in clinic 6 days after discharge and reconciled the medication list, restarting the olanzapine that the patient had stopped a few weeks before and the mirtazapine, which had not been restarted despite its presence on the discharge orders and patient instructions. She continued to have poor appetite and mood and was taking her medications only with great effort from her visiting nurse and staff at the retirement community. A major cause of this decline was the significant worsening of her depression brought on by hospitalization, lapses in her psychiatric medications, and emotional distress induced by the loss of her dentures during her hospital stay. She was readmitted 10 days after her discharge because she was unable to care for herself.

DISCUSSION

This case demonstrates numerous pitfalls in the transition process. Despite communication between the hospitalists and the PCP and a common electronic medical record, this patient failed the transition from the acute care hospital to the ambulatory setting. On the holiday weekend, ancillary support services were unavailable, including case management to contact her home care agency and her pharmacy to fill and deliver her new prescriptions. Despite efforts by the discharging physician, the out‐of‐town family could not be contacted. Thus, an elderly woman with cognitive impairment was left to process a new diagnosis and 7 medication changes with an unreliable mechanism to obtain her new medications.

With the rise of hospital medicine, it has increasingly been recognized that transitions represent a point of vulnerability in the care of geriatric patients. A change in physical location of care and handoffs between caregivers create the potential for error and loss of information. Prior research has demonstrated frequent quantitative and qualitative deficiencies in the information conveyed between inpatient and outpatient physicians, with direct communication occurring less than 20% of the time.1 In this case, communication occurred between the hospitalists and the outpatient physician, demonstrating that communication is just one element of successful transitions.

Components of effective care transitions have been described in the literature, including: preparation of the patient and caregiver for the transition, medication reconciliation, instructions to patient and caregiver about symptoms and signs of worsening, and an explicit follow‐up plan for tests and appointments.2 Optimally, there is interactive discussion between the hospitalist and the receiving clinician with a summary of events including an updated medication, allergy, and problem list, current advance directives, and a common plan of care.2 This case illustrates that these elements are necessary but may not be sufficient.

Some interventions have been found to be effective. A nurse‐led multidisciplinary approach to the discharge of elderly patients with congestive heart failure led to decreased readmission rates after 90 days and was found to be a cost‐saving measure.3 Similar results have been seen in geriatric patients with a variety of diagnoses in trials using advanced‐practice nurses to bridge the vulnerable period of discharge or by interventions to improve the ability of family caregivers to handle the challenges of the transition.46 Individualized attention to the unique needs of each patient and members of their social support structure, and investment in resources to do so, has the ability to decrease readmissions.

Medication errors, medication omissions, or the inability to fill medications on discharge represent a patient safety challenge. There has been increasing emphasis on medication reconciliation at admission and discharge, but in some cases the gold standard medication list is hard to determine. Electronic medical records would seem to be a natural solution to this problem, but as this case illustrates, the electronic record may not reflect the reality of patient adherence. As in this case, clarification may require another visit with the primary provider, leaving a period of time with an uncertain medication list and therefore a vulnerable patient. Access to medications after discharge was also a problem in this case, but this is not rare. A 2001 study found that 2 days after discharge from a general medicine hospital service, 1 in 5 patients had been unable to obtain all discharge medications.7 A pharmacist‐led medication reconciliation intervention in nursing home patients led to decreases in length of stay and discrepancy‐related adverse drug events. Furthermore, a follow‐up call allowed for clarification of medication questions in 25% of cases.7, 8

Patient characteristics such as depression and cognitive dysfunction have been found to affect readmission rates and are important to assess in addressing risk for poor outcomes after discharge. A 2000 study comparing readmission rates after discharge from a geriatric rehabilitation hospital found that patients with depression had an odds ratio of 3.5 for readmission compared with those without depression.9 Inadequate health literacy is also associated with decreased ability to self‐manage chronic disease and is associated with increased risk of mortality in community‐dwelling elderly such as the patient in this case.10 Asking patients or their proxies to explain their own understanding of the discharge plan can unmask comprehension issues that otherwise may go undetected.

Discharge on a weekend presents a period of critical vulnerability. Early recognition that a transition is susceptible to failure allows the events necessary for success to occur during the week when services are available. An example in the present case might include having had the pharmacy fill the prescriptions prior to the day of discharge. This does introduce a new opportunity for error in cases in which the plan of care changes but would have solved the inability to have prescriptions filled once the holiday weekend had begun.

In cases in which the usual mechanisms break down, increased effort on the part of the hospitalist can usually create a unique solution to the problem. Examples of creative solutions that did not occur in this case might include contacting the manager of the patient's retirement apartment to determine if this individual might be willing to fill prescriptions at an alternate pharmacy. A better alternative would be to change the system such that the solution is readily accessible and time efficient. Weekend availability of case management would be one such step. A means for the hospital's inpatient pharmacy to provide 2‐3 days of bridging medications would prevent weekend prescription access from affecting timely discharges of multiple patients over the course of a year. The hospitalist is in a unique position to take a leadership role in effecting system change to address these issues.

Ultimately, it is the duty of the hospitalist to take responsibility for the safety and well‐being of the patient, and if no solution can be found, it may be necessary to hold discharge or find an alternate disposition until logistical hurdles have been overcome. Indeed, for patients admitted for myocardial infarction, discharges were less likely to occur on weekends, presumably because of lack of ancillary services.11 With foresight, creative problem solving, and systems improvement, this should rarely be necessary.

Transitions continue to be a difficult time for the most vulnerable patients. Intense efforts have improved outcomes in selected populations but have not been broadly applied. Identification of patients at the highest risk, such as those with depression, poor social support, and cognitive limitations, would allow anticipation of difficult transitions and potential utilization of proven interventions, such as advanced‐practice nurses or follow‐up pharmacy contact. Processes such as these might have prevented some of the problems in this patient's discharge. Appreciation of the weekend discharge as a time of particular challenges allows barriers to be identified and solutions created during the week, when resources are still available. Attention to all elements of effective transitions should become part of the growing culture of patient safety.