Is minimally invasive parathyroid surgery an option for patients with gestational primary hyperparathyroidism?

BACKGROUND: Gestational primary hyperparathyroidism is associated with serious maternal and neonatal complications, which require prompt surgical treatment. Minimally invasive parathyroidectomy reduces pain, improves cosmesis and may achieve cure rates comparable to traditional open bilateral neck exploration. We report the clinical course of a woman with newly diagnosed gestational primary hyperparathyroidism and discuss the decision making behind the choice of video-assisted minimally invasive parathyroidectomy, amongst the other minimally invasive parathyroidectomy techniques available. CASE PRESENTATION: A 38-years-old pregnant woman at 9 weeks of gestation, with severe hyperemesis and hypercalcaemia secondary to gestational primary hyperparathyroidism (ionised calcium 1.28 mmol/l) was referred for surgery. Ultrasound examination of her neck identified 2 suspicious parathyroid enlargements. In view of pregnancy, a radioisotope Sestamibi parathyroid scan was not performed. Bilateral four-gland exploration was therefore deemed necessary to guarantee cure. This was performed with video-assisted minimally invasive parathyroidectomy, which relies on a single 15 mm central incision with external retraction and endoscopic magnification, allowing bilateral neck exploration. CONCLUSION: Video-assisted minimally invasive parathyroidectomy allows bilateral four-gland exploration, and is an optimal technique to treat gestational primary hyperparathyroidism. This procedure removes the need for radiation exposure, reduces pain, improves cosmesis and may achieve cure rates comparable to traditional open bilateral neck exploration.

Atorvastatin Metabolite Pattern in Skeletal Muscle and Blood from Patients with Coronary Heart Disease and Statin-Associated Muscle Symptoms.

Self-perceived statin-associated muscle symptoms (SAMS) are prevalent, but only a minority is drug-dependent. Diagnostic biomarkers are not yet identified. The local statin exposure in skeletal muscle tissue may correlate to the adverse effects. We aimed to determine whether atorvastatin metabolites in blood reflect the corresponding metabolite levels in skeletal muscle, and whether genetic variants of statin transporters modulate this relationship. We also addressed atorvastatin metabolites as potential objective biomarkers of SAMS. Muscle symptoms were examined in patients with coronary disease and self-perceived SAMS during 7 weeks of double-blinded treatment with atorvastatin 40 mg/day and placebo in randomized order. A subset of 12 patients individually identified with more muscle symptoms on atorvastatin than placebo (confirmed SAMS) and 15 patients with no difference in muscle symptom intensity (non-SAMS) attended the present follow-up study. All received 7 weeks of treatment with atorvastatin 40 mg/day followed by 8 weeks without statins. Biopsies from the quadriceps muscle and blood plasma were collected after each treatment period. Strong correlations (rho > 0.7) between muscle and blood plasma concentrations were found for most atorvastatin metabolites. The impact of the SLCO1B1 c.521T>C (rs4149056) gene variant on atorvastatin's systemic pharmacokinetics was translated into muscle tissue. The SLCO2B1 c.395G>A (rs12422149) variant did not modulate the accumulation of atorvastatin metabolites in muscle tissue. Atorvastatin pharmacokinetics in patients with confirmed SAMS were not different from patients with non-SAMS. In conclusion, atorvastatin metabolite levels in skeletal muscle and plasma are strongly correlated, implying that plasma measurements are suitable proxies of atorvastatin exposure in muscle tissue. The relationship between atorvastatin metabolites in plasma and SAMS deserves further investigation.

Trauma patients with prehospital Glasgow Coma Scale less than nine: not a homogenous group.

PURPOSE: Prehospital guidelines stratify and manage patients with Glasgow Coma Scale (GCS) less than nine and any sign of head injury as affected by severe traumatic brain injury (STBI). We hypothesized that this group of patients is so inhomogeneous that uniform treatment guidelines cannot be advocated. METHODS: Patients (2005-2012) with prehospital GCS below nine and abbreviated injury scale head and neck above two were identified from trauma registry. Patients with acute lethal injuries, isolated neck injuries, extubated within 24 h or transferred interhospitally were excluded. Patients were dichotomized based on the worst prehospital GCS (recorded before sedatives) into two groups: GCS 3-5 and GCS 6-8. These were statistically compared using univariate analysis. RESULTS: The GCS 3-5 group (99 patients) when compared with the GCS 6-8 group (49 patients) had shorter prehospital times (63 vs. 79 min; p < 0.05), more frequent episodes of both hypoxia (30.3% vs. 7.7%; p < 0.05) and hypotension (26.7% vs. 6.4%; p < 0.05), more often required craniectomy (15.1% vs. 4.0%; p = 0.05) and higher mortality (33.3% vs. 2%; p < 0.05). In the GCS 3-5 group, prehospital endotracheal intubation was attempted more often (57.5% vs. 28.6%, p < 0.05) and was more often successful (39.3% vs. 10.2%; p = 0.05). Length of stay in ICU did not differ. CONCLUSIONS: STBI patients are fundamentally different based on whether their initial GCS falls into 3-5 or 6-8 category. Recommendations from trials investigating trauma patients with GCS less than nine as one group should be translated with caution to clinical practice.

A tale of two cities: prehospital intubation with or without paralysing agents for traumatic brain injury.

BACKGROUND: The role of prehospital endotracheal intubation (PETI) for traumatic brain injury is unclear. In Victoria, paramedics use rapid sequence induction (RSI) drugs to facilitate PETI, while in New South Wales (NSW) they do not have access to paralysing agents. We hypothesized that RSI would both increase PETI rates and improve mortality. METHODS: Retrospective comparison of adult primary admissions (Glasgow Coma Scale <9 and abbreviated injury scale head and neck >2) to either Victorian or NSW trauma centre, which were compared with univariate and logistic regression analysis to estimate odds ratio for mortality and intensive care unit (ICU) length of stay. RESULTS: One hundred and ninety-two Victorian and 91 NSW patients did not differ in: demographics (males: 77% versus 79%; P = 0.7 and age: 34 (18-88) versus 33 (18-85); P = 0.7), Glasgow Coma Scale (3 (3-8) versus 5 (3-8); P = 0.07), and injury severity score (38 (26-75) versus 35 (18-75); P = 0.09), prehospital hypotension (15.4% versus 11.7%; P = 0.5) and desaturation (14.6% versus 17.5%; P = 0.5). Victorians had higher abbreviated injury scale head and neck (5 (4-5) versus 5 (3-6); P = 0.04) and more often successful PETI (85% versus 22%; P < 0.05). On logistic regression analysis, mortality did not differ among groups (31.7% versus 26.3%; P = 0.34; OR = 0.84; 95% CI: 0.38-1.86; P = 0.67). Among survivors, Victorians had longer stay in ICU (364 (231-486) versus 144 (60-336) h), a difference that persisted on gamma regression (effect = 1.58; 95% CI: 1.30-1.92; P < 0.05). CONCLUSION: Paramedics using RSI to obtain PETI in patients with traumatic brain injury had a higher success rate. This increase in successful PETI rate was not associated with an improvement in either mortality rate or ICU length of stay.

Brain CT perfusion provides additional useful information in severe traumatic brain injury.

BACKGROUND: The role of brain CT perfusion (CTP) imaging in severe traumatic brain injury (STBI) is unclear. We hypothesised that in STBI early CTP may provide additional information beyond the non contrast CT (NCCT). METHODS: Subset analysis of an ongoing prospective observational study on trauma patients with STBI who did not require craniectomy and deteriorated or failed to improve neurologically during the first 48h from trauma. Subsequently to follow-up NCCT, a CTP was obtained. Additional findings were defined as an area of altered perfusion on CTP larger than the abnormal area detected by the simultaneous NCCT. Patients who had additional finding (A-CTP) were compared with patients who did not have additional findings (NA-CTP). RESULTS: Study population was 30 patients [male: 90%, mean age: 38.6 (SD 16.9), blunt trauma: 100%; prehospital intubation: 6 (20%); lowest GCS before intubation: 5.1 (SD 2.0); mean ISS: 30.5 (SD 8.3); mean head and neck AIS: 4.4 (SD 0.8). Days in ICU: 10.2 (SD 6.3). Intracranial pressure (ICP) monitored in 12 (40%). Mean highest ICP in mmHg: 30.1 (SD14.1). There were five (17%) deaths. Findings of NCCT: primarily diffuse axonal injury (DAI) pattern in seven (23%), primarily haematoma in ten (33%), and primarily intracerebral contusion in nine (30%). CTP was performed 24.9 (SD 13) hours from trauma. There were 18 (60%) patients in the A-CTP group and 12 (40.0%) in NA-CTP. The A-CTP group was older (41.7 (SD16.9) vs 27.7 (SD 12.8): P<0.02) and showed on admission NCCT presence of cerebral contusion and absence of DAI. The degree of hypoperfusion was found to be severe enough to be in the ischaemic range in eight patients (27%). CTP altered clinical management in three patients (10%), who were diagnosed with massive and unsurvivable strokes despite minimal changes on NCCT. CONCLUSION: When compared to NCCT, CTP provided additional diagnostic information in 60% of patients with STBI. CTP altered clinical management in 10% of patients.

Strangulated intercostal liver herniation subsequent to blunt trauma. First report with review of the world literature.

Traumatic transdiaphragmatic intercostal hernia, defined as an acquired herniation of abdominal contents through disrupted intercostal muscles, is a rarely reported entity. We present the first reported case of a traumatic transdiaphragmatic intercostal hernia complicated by strangulation of the herniated visceral contents.Following blunt trauma, a 61-year old man developed a traumatic transdiaphragmatic intercostal hernia complicated by strangulation of liver segment VI. Due to pre-existing respiratory problems and the presence of multiple other injuries (grade III kidney laceration and lung contusion) the hernia was managed non-operatively for the first 2 weeks.The strangulated liver segment eventually underwent ischemic necrosis. Six weeks later the resulting subcutaneous abscess required surgical drainage. Nine months post injury the large symptomatic intercostal hernia was treated with laparoscopic mesh repair. Twelve months after the initial trauma, a small recurrence of the hernia required laparoscopic re-fixation of the mesh.This paper outlines important steps in managing a rare post traumatic entity. Early liver reduction and hernia repair would have been ideal. The adopted conservative approach caused liver necrosis and required staged procedures to achieve a good outcome.