Cerebral blood flow decreases during intermittent hemodialysis in patients with acute kidney injury, but not in patients with end-stage renal disease.

BACKGROUND: Cerebral blood flow (CBF) may decrease during intermittent hemodialysis (IHD). Patients with acute kidney injury (AKI) may be more vulnerable to cerebral hypoperfusion than patients with end-stage renal disease (ESRD), due to concomitant critical illness and hemodynamic instability. METHODS: In this observational, prospective study, we measured mean flow velocity at the level of the middle cerebral artery by transcranial Doppler at the start, after 2 h and at the end of a hemodialysis session in 15 consecutive patients with AKI and critical illness referred to the nephrological intensive care unit of a university hospital and in 12 patients with ESRD on regular treatment thrice weekly, who served as controls. We compared end-dialysis changes from baseline in mean flow velocity between the study groups and examined the correlation between this change and that of other relevant clinical parameters. RESULTS: Mean flow velocity decreased significantly at end-dialysis in the patients with AKI, but not in those with ESRD (P = 0.02). This difference persisted after adjusting for baseline mean flow velocity and net ultrafiltration volume. No significant correlations were found in either group between changes in mean flow velocity and changes in mean blood pressure (AKI: r = -0.27, P = 0.34; ESRD: r = 0.15, P = 0.68), SUN (AKI: r = -0.33, P = 0.25; ESRD: r = 0.06, P = 0.85), plasma HCO(3)(-) (AKI: r = -0.52, P = 0.24; ESRD: r = -0.18, P = 0.59), hematocrit (AKI: r = 0.08, P = 0.71; ESRD: r = -0.19, P = 0.65) or arterial oxygen content (AKI: r = -0.17, P = 0.36; ESRD: r = -0.33, P = 0.43). CONCLUSIONS: Our data suggest that AKI patients may be more vulnerable than ESRD patients to cerebral hypoperfusion during IHD. Our findings do not support a clear-cut role of rapid changes in blood osmolarity, rheological properties or vasoreactivity of the cerebral circulation to O(2) supply in modulating CBF during hemodialysis.

Gait analysis in patients undergoing ACL reconstruction according to Kenneth Jones' technique.

The anterior cruciate ligament is essential for knee stability, and its injury, both acute and in the case of chronic knee instability, promotes meniscal degenerative alterations, as well as the onset and progression of gonarthrosis. In this retrospective study, young adults engaged in nonprofessional sportive activities undergoing ACL reconstruction by the Kenneth-Jones technique were assessed clinically and with gait analysis, to detect any deficits persisting even after rehabilitation at a follow- up of approximately 6 months. Eight patients who had undergone elective ligament reconstruction by Kenneth-Jones were assessed between the 5th and 7th month postsurgery with clinical-anamnestic investigation, including the Hughston Clinic subjective knee questionnaire and by gait analysis with the EL.I.Te. system. Gait analysis showed a reduction of ACL protection mechanisms during initial stance; furthermore, the operated limb globally exhibited greater difficulty in muscle recruitment. Residual deficits in muscle recruitment, exposing the reconstructed ligament to possible injuries, persist after a rehabilitation program and after resuming ofpre-surgery activities, thus adjustment of the rehabilitative program on the basis of these findings is recommended.

Renal resistive index by transesophageal and transparietal echo-doppler imaging for the prediction of acute kidney injury in patients undergoing major heart surgery.

BACKGROUND: Acute kidney injury (AKI) following major heart surgery (MHS) is associated with early decrease in renal blood flow and worsened prognosis. Doppler-derived renal resistive index (RRI), which reflects renal vascular resistance, may predict the development of AKI in patients undergoing MHS. METHODS: We studied 60 consecutive patients (mean age 69.5 years, range 30-88, 41 males) undergoing MHS. We measured RRI, both at the renal sinus and intraparenchymally, by transesophageal echo-Doppler ultrasound (TE-EDus) at anesthesia induction and at the end of surgery in all patients. Additionally, we measured RRI by external transparietal echo-Doppler ultrasound (TP-EDus) at the following time points: anesthesia induction, end of surgery, 4 and 24 h from cardiopulmonary bypass (CPB) start. We also measured serum neutrophil gelatinase associated lipocalin (NGAL) at the same time points. RESULTS: AKI [serum creatinine (sCr) increase ≥0.3 mg/dl vs. baseline within 72 h] developed in 23/60 (38.3 %) patients, with two requiring dialysis. Systemic hemodynamic parameters were similar in the patients who developed AKI (AKI+) and in those who did not (AKI-). Intraparenchymal RRI at end-surgery was significantly higher in AKI+ compared to AKI- patients, both at TE-EDus and TP-EDus (TE-EDus mean difference, p = 0.004; TP-EDus mean difference, p = 0.013; difference between TE-EDus and TP-EDus results, p = 0.066), although the predictive performance was limited with both methods (area under the curve [AUC] of the receiver-operator characteristics: 0.71 and 0.70 for TE-EDus and TP-EDus, respectively). Serum NGAL values were higher in AKI + than in AKI- patients (anesthesia induction, p = 0.037; end-surgery, p = 0.007; 4 h from CPB start, p = 0.093; 24 h from CPB start, p = 0.024. However, combining RRI with serum NGAL at end-surgery did not provide a clear-cut advantage in predicting AKI. CONCLUSIONS: In patients undergoing MHS, increased echo-Doppler ultrasound-derived RRI at end-surgery is significantly associated with the risk of AKI, but has limited practical utility for identifying the patients who will develop AKI.

[Hyponatremia in clinical practice]. / L'iponatremia nella pratica clinica.

Hyponatremia is the most frequent electrolyte disorder in hospitalized patients and it is associated with unfavorable clinical outcomes as well as increased hospital costs. Its clinical presentation may be highly variable, ranging from asymptomaticity to neurologic emergencies with seizures or coma as signs of rapidly worsening cerebral edema. In these cases, prompt treatment is mandatory to avoid the patients death. On the other hand, in the case of gradual development of hyponatremia, it is imperative that its correction be also appropriately slow in order to avoid another neurological catastrophe, namely the osmotic demyelination syndrome. Whilst recent international guidelines and expert consensus agree on the approach to the treatment of acute severe and symptomatic hyponatremia, the recommendations on pharmacological therapy in chronic hyponatremia diverge, particularly as to the potential use of vasopressin antagonists. This review is aimed at summarizing essential aspects of epidemiology, pathophysiology and the diagnostic process of hyponatremia, to set the ground for a practical as well as evidence-based approach to treatment. As a guide through the discussion of the available evidence, a clinical case is presented in which the patients history and laboratory data are crucial for identifying the etiology of hyponatremia. The severe neurological signs at presentation justify an emergency treatment with hypertonic saline, as indicated. Subsequently, as the neurological emergency subsides, we discuss the need to revert the trend towards hypercorrection by an apparently counterintuitive approach, based in fact on sound pathophysiological grounds, with continuous infusion of hypotonic solutions and administration of desmopressin.

Total knee replacement. Postacute phase in rehabilitation: objectives and strategies in postacute treatment.

Identification of a population with homogeneous characteristics is the fundamental introduction to elaborate a rehabilitation plan after operation of total knee arthroplasty (TKA). The main objectives of our rehabilitative protocol are: improvement of the preoperative clinical state, prevention and management of the common postoperative problems and complications. The first objective requires the improvement of the function of the operated knee (good articular excursion, muscular strengthening and recovery of ambulation and of gait pattern), as well as the reduction of pain. These protocol objectives are progressively achieved spreading postoperative rehabilitative strategies into four stages, during which patient should take instruction about the adoption of a correct life style.

Cerebral perfusion during intermittent hemodialysis in patients with acute kidney injury and advanced liver cirrhosis.

BACKGROUND: Cerebral blood flow (CBF) decreases during intermittent hemodialysis (HD) in patients with acute kidney injury (AKI). Since cerebral hemodynamics may be impaired in liver cirrhosis (LC), this condition could aggravate cerebral hypoperfusion during HD in patients with AKI. We examined CBF during the first HD session in patients admitted for AKI, with or without LC. METHODS: CBF was examined by measuring middle cerebral artery mean flow velocity (MCAmfv) with transcranial Doppler at baseline and at the end of the first 4-hour HD session in 11 patients with both AKI and LC (median age 69 years, range 40-87, 7 men). Eleven patients with AKI without LC (median age 77 years, range 69-92, 6 men) served as controls. RESULTS: Median net ultrafiltration volume at the end of the HD session was slightly, albeit not significantly, smaller in the patients with LC than in those without (-0.25 kg [range 0.00 to -1.50] vs. -1.00 kg [range 0.00 to -2.00], p = 0.18). At end of HD session, median MCAmfv had decreased by -5.5 cm/s (range -41.3 to 9.9) in the patients with LC, and by -4.5 cm/s (range -11.0 to -2.5) in those without LC (p = 0.79). At end of HD session, the mean MCAmfv of the 2 groups, adjusted for baseline MCAmfv and net ultrafiltration volume, was 25.7 and 21.1 cm/s in AKI patients with and without LC, respectively (difference between groups: 4.6 cm/sec; 95% confidence interval, -3.8 to +13.0). CONCLUSION: In patients with AKI, concomitant LC does not confer greater vulnerability to cerebral hypoperfusion during intermittent HD.

Efficacy and safety of a citrate-based protocol for sustained low-efficiency dialysis in AKI using standard dialysis equipment.

BACKGROUND AND OBJECTIVES: A simple anticoagulation protocol was developed for sustained low-efficiency dialysis (SLED) in patients with AKI, based on the use of anticoagulant citrate dextrose solution formulation A (ACD-A) and standard dialysis equipment. Patients' blood recalcification was obtained from calcium backtransport from dialysis fluid. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: All patients treated with SLED (8- to 12-hour sessions) for AKI in four intensive care units of a university hospital were studied over a 30-month period, from May 1, 2008 to September 30, 2010. SLED interruptions and their causes, hemorrhagic complications, as well as coagulation parameters, ionized calcium, and blood citrate levels were recorded. RESULTS: This study examined 807 SLED sessions in 116 patients (mean age of 69.7 years [SD 12.1]; mean Acute Physiology and Chronic Health Evaluation II score of 23.8 [4.6]). Major bleeding was observed in six patients (5.2% or 0.4 episodes/100 person-days follow-up while patients were on SLED treatment). Citrate accumulation never occurred, even in patients with liver dysfunction. Intravenous calcium for ionized hypocalcemia (< 3.6 mg/dl or < 0.9 mmol/L) was needed in 28 sessions (3.4%); in 8 of these 28 sessions (28.6%), low ionized calcium was already present before SLED start. In 92.6% of treatments, SLED was completed within the scheduled time (median 8 hours). Interruptions of SLED by impending/irreversible clotting were recorded in 19 sessions (2.4%). Blood return was complete in 98% of the cases. In-hospital mortality was 45 of 116 patients (38.8%). CONCLUSIONS: This study protocol affords efficacious and safe anticoagulation of the SLED circuit, avoiding citrate accumulation and, in most patients, systematic calcium supplementation; it can be implemented with commercial citrate solutions, standard dialysis equipment, on-line produced dialysis fluid, and minimal laboratory monitoring.

Upper and lower cluster headache: clinical and pathogenetic observations in 608 patients.

UNLABELLED: OBJECTIVE, BACKGROUND, AND METHODS: Ever since it was proposed by Ekbom and Kugelberg back in 1968 on the basis of the different location of head pain during attacks, the differentiation of cluster headache into an upper syndrome (US) and a lower syndrome (LS) has been regarded as a purely academic distinction. To evaluate whether this differentiation is indeed well founded and to understand its possible significance in the light of current pathogenetic knowledge, we rigorously applied Ekbom and Kugelberg's classification criteria to a sample of 608 patients with cluster headache (CH; 440 men and 168 women), including 483 with episodic CH, 69 with chronic CH, and 56 with CH periodicity undetermined. RESULTS: Of these patients, 278 could be classified as US sufferers and 330 as LS sufferers. Our data analysis showed statistically significant clinical differences between the two syndromes: pain location was more common in the ocular, temporal, and nuchal regions among LS sufferers; in addition, patients with LS reported not only a higher rate of autonomic symptoms, but also a higher predominance of nasal congestion, ptosis, and forehead and facial sweating among these symptoms. CONCLUSIONS: Based on current anatomofunctional knowledge and on the most recent pathogenetic findings, we believe that changes in hypothalamic activity posteroinferiorly may lead to activation of the caudal part of the spinal trigeminal nucleus by way of the hypothalamus, midbrain, and trigeminal nerve fibers and consequently to activation of the trigeminovascular system with a different location in the two syndromes. More specifically, there seems to be a larger and more extensive involvement of the subnucleus caudalis in LS compared with US, where only its ventrocaudal portions are likely to be affected.