Exploring newly qualified doctors' workplace stressors:an interview study from Australia

Purpose Postgraduate year 1 (PGY1) doctors suffer from high levels of psychological distress, yet the contributory factors are poorly understood. This study used an existing model of workplace stress to explore the elements most pertinent to PGY1 doctors. In turn, the data were used to amend and refine the conceptual model to better reflect the unique experiences of PGY1 doctors. Method Focus groups were undertaken with PGY1 doctors working at four different health services in Victoria, Australia. Transcripts were coded using Michie's model of workplace stress as the initial coding template. Remaining text was coded inductively and the supplementary codes were used to modify and amplify Michie's framework. Results There were 37 participants in total. Key themes included stressors intrinsic to the job, such as work overload and long hours, as well as those related to the context of work such as lack of role clarity and relationships with colleagues. The main modification to Michie's framework was the addition of the theme of uncertainty. This concept related to most of the pre-existing themes in complex ways, culminating in an overall sense of anxiety. Conclusions Michie's model of workplace stress can be effectively used to explore the stressors experienced by PGY1 doctors. Pervasive uncertainty may help to explain the high levels of psychological morbidity in this group. While some uncertainty will always remain, the medical education community must seek ways to improve role clarity and promote mutual respect.</p

Exploring newly qualified doctors' workplace stressors:an interview study from Australia

Purpose Postgraduate year 1 (PGY1) doctors suffer from high levels of psychological distress, yet the contributory factors are poorly understood. This study used an existing model of workplace stress to explore the elements most pertinent to PGY1 doctors. In turn, the data were used to amend and refine the conceptual model to better reflect the unique experiences of PGY1 doctors. Method Focus groups were undertaken with PGY1 doctors working at four different health services in Victoria, Australia. Transcripts were coded using Michie's model of workplace stress as the initial coding template. Remaining text was coded inductively and the supplementary codes were used to modify and amplify Michie's framework. Results There were 37 participants in total. Key themes included stressors intrinsic to the job, such as work overload and long hours, as well as those related to the context of work such as lack of role clarity and relationships with colleagues. The main modification to Michie's framework was the addition of the theme of uncertainty. This concept related to most of the pre-existing themes in complex ways, culminating in an overall sense of anxiety. Conclusions Michie's model of workplace stress can be effectively used to explore the stressors experienced by PGY1 doctors. Pervasive uncertainty may help to explain the high levels of psychological morbidity in this group. While some uncertainty will always remain, the medical education community must seek ways to improve role clarity and promote mutual respect.</p

When the Problem Becomes the Solution - Video

25 year-old man noticed slow progressive decrease in vision in left eye. Vision was 20/20 OD and 20/40 OS, there was swelling of left optic nerve head. MRI demonstrated white matter lesions in left frontal lobe; cerebrospinal fluid composition was normal. Patient was seen in MS clinic and treatment with dimethyl fumarate commenced. Vision continued to deteriorate and when seen by neuro-ophthalmology service 4 months later it was 20/200 in affected eye with brisk left RAPD and dramatically swollen left optic nerve head. Urgent MRV was interpreted as normal and MRI demonstrated white matter changes in deep left frontal lobe, felt to be microischemic, not demyelinating. Dimethyl fumarate was discontinued; serological workup (HIV, Lyme, Toxoplasma, Bartonella, VDRL, ACE, ANA, ds-DNA, ENA and NMO testing) was unrevealing. CT body was normal. Vision remained stable. Dramatic swelling of left optic nerve persisted as he was followed over 2 years. 2.5 years after initial presentation the patient experienced sudden seizure. MRI demonstrated mass lesion surrounded by edema in left frontal lobe. After transfer to our center biopsy of the lesion was interpreted as "indeterminate" but negative for neoplasm. Second opinion on the biopsy commented on findings inconsistent with both demyelination and arterial infarct. Cerebral Angiography (angiogram) reported unusual tortuous left hemispheric cortical veins without arteriovenous shunting lesion. After extensive multidisciplinary consultation, neurosarcoidosis was felt to be a unifying diagnosis despite absence of tissue diagnosis proving it. Treatment with intravenous methylprednisolone and mycophenolate commenced. MRI done 2 months after starting immunosuppression demonstrated dramatic resolution of the left frontal lobe lesion. Unsatisfied with the diagnosis, all neuro-imaging was re-reviewed. On angiogram the unusual tortuous cortical veins in the left hemisphere were reminiscent of the "pseudophlebitic pattern" seen with brain dural AV fistula (BDAVF). Diagnostic procedure was performed

When the Problem Becomes the Solution - Slides

25 year-old man noticed slow progressive decrease in vision in left eye. Vision was 20/20 OD and 20/40 OS, there was swelling of left optic nerve head. MRI demonstrated white matter lesions in left frontal lobe; cerebrospinal fluid composition was normal. Patient was seen in MS clinic and treatment with dimethyl fumarate commenced. Vision continued to deteriorate and when seen by neuro-ophthalmology service 4 months later it was 20/200 in affected eye with brisk left RAPD and dramatically swollen left optic nerve head. Urgent MRV was interpreted as normal and MRI demonstrated white matter changes in deep left frontal lobe, felt to be microischemic, not demyelinating. Dimethyl fumarate was discontinued; serological workup (HIV, Lyme, Toxoplasma, Bartonella, VDRL, ACE, ANA, ds-DNA, ENA and NMO testing) was unrevealing. CT body was normal. Vision remained stable. Dramatic swelling of left optic nerve persisted as he was followed over 2 years. 2.5 years after initial presentation the patient experienced sudden seizure. MRI demonstrated mass lesion surrounded by edema in left frontal lobe. After transfer to our center biopsy of the lesion was interpreted as "indeterminate" but negative for neoplasm. Second opinion on the biopsy commented on findings inconsistent with both demyelination and arterial infarct. Cerebral Angiography (angiogram) reported unusual tortuous left hemispheric cortical veins without arteriovenous shunting lesion. After extensive multidisciplinary consultation, neurosarcoidosis was felt to be a unifying diagnosis despite absence of tissue diagnosis proving it. Treatment with intravenous methylprednisolone and mycophenolate commenced. MRI done 2 months after starting immunosuppression demonstrated dramatic resolution of the left frontal lobe lesion. Unsatisfied with the diagnosis, all neuro-imaging was re-reviewed. On angiogram the unusual tortuous cortical veins in the left hemisphere were reminiscent of the "pseudophlebitic pattern" seen with brain dural AV fistula (BDAVF). Diagnostic procedure was performed

When the Problem Becomes the Solution - Abstract

25 year-old man noticed slow progressive decrease in vision in left eye. Vision was 20/20 OD and 20/40 OS, there was swelling of left optic nerve head. MRI demonstrated white matter lesions in left frontal lobe; cerebrospinal fluid composition was normal. Patient was seen in MS clinic and treatment with dimethyl fumarate commenced. Vision continued to deteriorate and when seen by neuro-ophthalmology service 4 months later it was 20/200 in affected eye with brisk left RAPD and dramatically swollen left optic nerve head. Urgent MRV was interpreted as normal and MRI demonstrated white matter changes in deep left frontal lobe, felt to be microischemic, not demyelinating. Dimethyl fumarate was discontinued; serological workup (HIV, Lyme, Toxoplasma, Bartonella, VDRL, ACE, ANA, ds-DNA, ENA and NMO testing) was unrevealing. CT body was normal. Vision remained stable. Dramatic swelling of left optic nerve persisted as he was followed over 2 years. 2.5 years after initial presentation the patient experienced sudden seizure. MRI demonstrated mass lesion surrounded by edema in left frontal lobe. After transfer to our center biopsy of the lesion was interpreted as "indeterminate" but negative for neoplasm. Second opinion on the biopsy commented on findings inconsistent with both demyelination and arterial infarct. Cerebral Angiography (angiogram) reported unusual tortuous left hemispheric cortical veins without arteriovenous shunting lesion. After extensive multidisciplinary consultation, neurosarcoidosis was felt to be a unifying diagnosis despite absence of tissue diagnosis proving it. Treatment with intravenous methylprednisolone and mycophenolate commenced. MRI done 2 months after starting immunosuppression demonstrated dramatic resolution of the left frontal lobe lesion. Unsatisfied with the diagnosis, all neuro-imaging was re-reviewed. On angiogram the unusual tortuous cortical veins in the left hemisphere were reminiscent of the "pseudophlebitic pattern" seen with brain dural AV fistula (BDAVF). Diagnostic procedure was performed