Summary : This flowchart presents a comprehensive algorithm for the prevention and care of diabetic foot, including screening, ulcer management, wound care, offloading, infection and ischemia assessment, and advanced therapies. flowchart: # Nodes : • DFU Prevention (rounded rectangle): Patient education, annual foot exam, glycemic control (A1c<7%), therapeutic footwear, Semmes-Weinstein test, ABI at age 50, vascular risk factor management. • Patient developed ulcer (rectangle). • Assess for ischemia, infection and neuropathy (rectangle): ABI + TcPO2, PTB + plain XR. • Comprehensive wound care (rectangle): Debridement and follow up q 1-4 wk, moist wound bed, control exudate, avoid maceration. • Offloading (rectangle). • Suspected soft tissue abscess or osteomyelitis (rectangle): MRI (if not possible, leukocyte or antigranulocyte scan + bone scan). • Clinically significant PAD (rectangle): Revascularization (either surgical bypass or endovascular therapy). • Healed (rectangle). • No response in 4 wks (rectangle): Adjunctive wound therapy (HBO, NPWT, cellular and extracellular agents). • plantar DFU (rectangle): Total contact cast or irremovable fixed ankle walking boot. • non-plantar (rectangle): Relieves pressure at the site of the ulcer. • Alternative for frequent dressing changes (rectangle): Removable cast. • Osteomyelitis (rectangle): Bone debridement, biopsy and culture, antibiotics, HBO. # Connectors : • Arrow from DFU Prevention to Patient developed ulcer. • Arrow from Patient developed ulcer to Assess for ischemia, infection and neuropathy. • From Assess for ischemia, infection and neuropathy, three branches: – To Comprehensive wound care. – To Offloading. – To Suspected soft tissue abscess or osteomyelitis and Clinically significant PAD. • Comprehensive wound care leads to Healed or, if no response in 4 wks, to adjunctive wound therapy. • Offloading splits into plantar DFU (total contact cast or irremovable boot) and non-plantar (relieves pressure at ulcer site), with alternative for frequent dressing changes (removable cast). • Suspected soft tissue abscess or osteomyelitis leads to Osteomyelitis (bone debridement, biopsy, antibiotics, HBO). • Clinically significant PAD leads to revascularization. • All branches ultimately aim for healing. # Layout : • Top-down flow, starting with prevention, then ulcer development, assessment, and branching into wound care, offloading, infection/ischemia management. • Multiple parallel branches for different clinical scenarios. • Merges at points where healing is achieved or advanced therapies are considered. # Analysis : • The flowchart emphasizes early prevention and regular screening to reduce diabetic foot ulcer (DFU) risk. • Once an ulcer develops, a systematic assessment for ischemia, infection, and neuropathy guides further management. • Wound care and offloading are central, with specific strategies for plantar and non-plantar ulcers. • Advanced imaging and therapies are reserved for cases with suspected infection or poor response to standard care. • The algorithm integrates vascular assessment and revascularization for patients with peripheral arterial disease (PAD). • The workflow is designed to optimize healing and minimize complications through stepwise escalation of care.

Summary : This flowchart presents an algorithm for the treatment of diabetic peripheral neuropathy (DPN), guiding clinicians through decision-making steps for pain management, agent selection, and escalation of care based on symptom persistence and medication tolerance. flowchart: # Nodes : • "Is pain due to DPN?" (hexagon) • "NO or not sure" (rectangle) • "Refer to neurology or pain clinic" (rectangle) • "YES" (rectangle) • "Assess comorbidities, costs, drug-drug interactions, potential for adverse effects ➔ choose one of the following agents" (rectangle) • "ANTICONVULSANTS Pregabalin* Gabapentin" (rectangle) • "SNRIs Duloxetine* Venlafaxine" (rectangle) • "TCAs Amitriptyline, Nortriptyline" (rectangle) • "Capsaicin* 8% patch" (rectangle) • "Exercise" (rectangle) • "Persistence of symptoms" (rectangle) • "Avoid Opioids!" (rectangle, orange) • "Switch to another agent from above" (rectangle) • "Try combining agents from above" (rectangle) • "Persistent pain/medication not tolerated" (rectangle) • "Refer to pain clinic" (rectangle) # Connectors : • Arrow from "Is pain due to DPN?" to "NO or not sure" and "YES". • Arrow from "NO or not sure" to "Refer to neurology or pain clinic". • Arrow from "YES" to "Assess comorbidities..." and then to five agent options: "ANTICONVULSANTS", "SNRIs", "TCAs", "Capsaicin* 8% patch", "Exercise". • Arrows from all five agent options to "Persistence of symptoms". • Arrow from "Persistence of symptoms" to "Avoid Opioids!", "Switch to another agent from above", and "Try combining agents from above". • Arrow from "Switch to another agent from above" and "Try combining agents from above" to "Persistent pain/medication not tolerated". • Arrow from "Persistent pain/medication not tolerated" to "Refer to pain clinic". # Layout : • Top-down, stepwise progression. • Initial decision node at top, branching to referral or treatment assessment. • Five parallel agent options in the middle. • Symptom persistence leads to further branching for agent switching, combination, or referral. • Orange highlight for "Avoid Opioids!" as a warning. # Additional Information : • Footnotes: *FDA approved for treatment of DSPN. • Abbreviations: DPN = diabetic peripheral neuropathy; DSPN = distal symmetrical polyneuropathy; FDA = Food and Drug Administration; SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant. • Source: Adapted from Pop-Busui, Boulton, et al, Diabetes Care 2017;40:136-154. # Analysis : • The algorithm prioritizes non-opioid agents for pain management in DPN, with anticonvulsants, SNRIs, TCAs, topical capsaicin, and exercise as first-line options. • If symptoms persist, clinicians are advised to avoid opioids, switch agents, or combine therapies. • Persistent pain or intolerance to medication prompts referral to a pain clinic. • The flowchart emphasizes assessment of comorbidities and adverse effects before agent selection, and provides clear escalation steps for refractory cases.

Summary : This flowchart provides a comprehensive management algorithm for adults with atopic dermatitis, detailing baseline management, topical therapies, phototherapy, and systemic therapies, including FDA-approved and recommended treatments, maintenance strategies, and escalation steps for inadequate control. flowchart: # Baseline Management : • Severity Assessment: Assessment of signs of disease, severity of symptoms, comorbidities, and impact on quality of life (QOL). • Exacerbating Factor Avoidance: Identify trigger factors (allergens, irritants, etc.) and counsel patients on avoidance. • Baseline Therapy: Moisturizers/Emollients (strong recommendation), Bathing Practices (conditional recommendation). # Initial Pathways : • Mild to Severe: Proceed to Topical Therapies. • Moderate to Severe: Proceed to Phototherapy & Systemic Therapy. # Topical Therapies : ## Optimized Topical Therapy for Inflamed Areas : • TCS (Topical corticosteroids) (FDA, strong recommendation) • TCIs (Topical calcineurin inhibitors) (FDA, strong recommendation) • Crisaborole ointment (FDA, strong recommendation) • Ruxolitinib cream (FDA, strong recommendation) • Wet Dressings (strong recommendation) ## Ongoing Maintenance with Topical Therapies : • Reactive or proactive application for maintenance. • Shared decision-making for long-term treatment. • Consider patient satisfaction and adherence. ## Inadequate Control : • If topical therapy and basic management optimized, consider alternative diagnoses. • Consider additional treatment with phototherapy and/or systemic agents. # Phototherapy & Systemic Therapy : • Topical agents can be used concurrently with phototherapy or systemic agents for maintenance, rescue, or flares. # Phototherapy : • No specific agents listed; included as a treatment option for moderate to severe cases. # Systemic Therapies : ## Biologics : • Dupilumab (FDA, strong recommendation) • Tralokinumab (FDA, strong recommendation) ## JAK Inhibitors : • Upadacitinib (FDA, strong recommendation) • Abrocitinib (FDA, strong recommendation) • Baricitinib (strong recommendation) ## Immunosuppressants : • Methotrexate (strong recommendation) • Azathioprine (strong recommendation) • Cyclosporine (strong recommendation) • Mycophenolate mofetil (strong recommendation) • Systemic corticosteroids (FDA, strong recommendation against use) # Key : • Green circle: Strong recommendation in favor. • Yellow circle: Conditional recommendation in favor. • Red circle: Strong recommendation against. • Orange circle: Conditional recommendation against. • FDA: Indicated for atopic dermatitis. # Abbreviations : • QOL: Quality of Life • FDA: Food and Drug Administration • TCS: Topical corticosteroids • TCI: Topical calcineurin inhibitor # Layout : • The flowchart is organized from baseline management at the top, splitting into two main pathways (mild to severe and moderate to severe), with further branches into topical, phototherapy, and systemic therapies. • Maintenance and escalation steps are included for ongoing management and inadequate control. # Analysis : • The algorithm emphasizes starting with baseline management and topical therapies, escalating to phototherapy and systemic therapies for more severe or refractory cases. • Strong recommendations are visually highlighted for first-line agents, with systemic corticosteroids strongly discouraged. • FDA-approved options are clearly marked, supporting evidence-based decision-making. • The flowchart supports a stepwise, patient-centered approach, integrating maintenance and escalation strategies.

Summary : This flowchart provides a clinical decision-making pathway for the management of diabetic patients with moderate (Grade 3) and severe (Grade 4) infections, focusing on hospitalisation, antibiotic therapy, surgical consultation, and osteomyelitis treatment. flowchart: # Grade 3: Person with diabetes and moderate infection Nodes : • Start (rectangle): "Person with diabetes and moderate infection GRADE 3" • Decision (rectangle): "Consider hospitalisation, especially if patient has multiple comorbidities" • Decision (rectangle): "Extensive gangrene, necrotising infection, deep abscess, penetrating injury or foreign body, compartment syndrome, severe lower limb ischaemia or probable osteomyelitis associated with soft tissue infection" • Decision (rectangle): "Probable osteomyelitis without soft tissue infection" • Process (rectangle): "Treat most patients with an oral antibiotic at presentation or after initial improvement taking into account modifying factors (see Box 1)" • Process (rectangle): "Treat empirically with broad spectrum oral antibiotics to cover Gram positive, common Gram negative and anaerobic pathogens (e.g. amoxicillin-clavulanate; see eTG1)" • Process (rectangle): "Consider using an agent active against Pseudomonas if it was isolated within the previous few weeks or for moderate infection in a tropical/subtropical climate" • Process (rectangle): "Consider MRSA cover (see Box 2)" • Process (rectangle): "Reconsider antibiotic regimen based on clinical response as well as culture and sensitivity results" • Process (rectangle): "For initial intravenous therapy, switch to oral antibiotics once patient is clinically improving" • Decision (rectangle): "Deep or extensive skin and soft tissue infection or severe peripheral artery disease" • Process (rectangle): "Continue antibiotics for 1-2 weeks total" • Process (rectangle): "Consider continuing antibiotics for 3-4 weeks total (review after 1-2 weeks)" • Decision (rectangle): "Clinical deterioration or failure to improve at clinical review or end of planned therapy" • Process (rectangle): "Re-evaluate and consider further diagnostic studies or alternative treatment (including for deep structure involvement, collections, resistant organisms or non-infectious pathology)" # Grade 4: Person with diabetes and severe infection Nodes : • Start (rectangle): "Person with diabetes and severe infection GRADE 4" • Process (rectangle): "Recommend hospitalisation and taking blood cultures" • Decision (rectangle): "Urgently consult with a surgical specialist to consider surgery" • Process (rectangle): "Treat empirically with an intravenous antibiotic covering Gram positive, common Gram negative and anaerobic pathogens and taking into account modifying factors (see Box 1; see eTG1)" • Process (rectangle): "Consider using an agent active against Pseudomonas if it was isolated within the previous few weeks or in a tropical/subtropical climate" • Process (rectangle): "Consider MRSA cover (see Box 2)" • Decision (rectangle): "Probable osteomyelitis" • Process (rectangle): "Treat with an appropriate empiric antibiotic; consider switching from intravenous to orally bioavailable antibiotics after 5-7 days if the likely or proven pathogen is susceptible" • Decision (rectangle): "Uncomplicated forefoot osteomyelitis" • Process (rectangle): "Consider treating with antibiotics alone" • Decision (rectangle): "If surgery performed, consider obtaining specimen from stump (proximal margin) of resected bone for culture AND histopathology" • Decision (rectangle): "Known residual osteomyelitis or culture/histopathology suggests residual osteomyelitis" • Process (rectangle): "Administer appropriate antibiotics for up to 6 weeks" • Decision (rectangle): "Concomitant soft tissue infection present" • Process (rectangle): "Treat with antibiotics for 2 to 5 days and then cease" Connectors : • Arrows indicate decision points (YES/NO) and direct flow to subsequent steps. • YES/NO branches are clearly marked at each decision node. • Some nodes loop back to earlier steps if clinical deterioration or failure to improve occurs. Layout : • Two parallel columns: left for Grade 3 (moderate infection), right for Grade 4 (severe infection). • Each column starts with initial assessment, then branches based on clinical findings and response to therapy. • Decision nodes and process steps are arranged vertically, with arrows connecting them according to clinical logic. Analysis : • The flowchart provides a structured approach for clinicians to manage diabetic infections, distinguishing between moderate and severe cases. • Emphasises early hospitalisation and surgical consultation for severe infections. • Antibiotic therapy is tailored based on infection severity, pathogen risk, and clinical response. • Osteomyelitis management includes both medical and surgical options, with clear criteria for duration and type of antibiotic therapy. • The chart highlights the importance of re-evaluation and diagnostic flexibility in cases of poor clinical response.

This diagnostic image shows a continuous fetal cardiotocography (CTG) tracing at 27 weeks of gestation, illustrating the impact and subsequent resolution of maternal diabetic ketoacidosis (DKA) on fetal well-being. The top panel displays the fetal heart rate (FHR) in beats per minute (bpm), while the bottom panel shows tocodynamometry (maternal uterine activity). The initial 30-minute segment (left side) demonstrates pathological features: a baseline tachycardia exceeding 160 bpm, significantly reduced baseline variability (flattened tracing), and repetitive variable decelerations characterized by sharp, transient drops in FHR. These findings are clinically significant as they reflect fetal stress or hypoxia secondary to maternal metabolic derangement. Following medical intervention (saline and insulin), the latter half of the tracing shows a clear normalization: the FHR baseline stabilizes around 150-160 bpm, normal beat-to-beat variability reappears, and decelerations resolve. This timeline-based progression serves as an educational example of how maternal acute illness affects fetal heart rate patterns and the rapid response to appropriate clinical stabilization.

Clinical photograph providing a lateral view of a male torso in an upright position, demonstrating severe insulin-induced lipohypertrophy. The image captures a prominent, circumscribed protrusion of subcutaneous adipose tissue in the lower lateral abdomen. This localized bulge disrupts the natural contour of the abdominal wall, presenting as a firm, raised mass several centimeters in diameter. The overlying skin appears intact and smooth, though it exhibits terminal hair growth consistent with the patient's demographics. Minor skin findings include scattered nevi and faint horizontal skin creases from posture. This visual serves as a classic clinical example of a common complication in patients with long-standing type 1 diabetes who repeatedly inject insulin into the same site. The educational focus is on the physical manifestation of lipohypertrophy, which can impair insulin absorption and lead to poor glycemic control, as seen in clinical scenarios like diabetic ketoacidosis (DKA).

This medical timeline chart is a Statistical Process Control (SPC) chart, specifically a longitudinal line graph illustrating the monthly frequency of Pediatric Intensive Care Unit (PICU) admissions for Diabetic Ketoacidosis (DKA) from January 2016 to December 2020. The chart features three horizontal reference lines: a solid central line representing the mean, and two dashed lines representing the Upper Control Limit (UCL) and Lower Control Limit (LCL). From early 2016 through mid-2019, the data exhibits common-cause variation, with admission numbers remaining stable and generally fluctuating below the mean, rarely approaching the LCL (approximately 5 admissions). A significant shift toward special-cause variation begins in late 2019. Starting around November 2019 and continuing through 2020, there is a sustained increase in both volume and volatility. Multiple data points in 2020 (notably around March, July, and August) exceed the UCL, peaking at over 30 admissions per month. This visual evidence demonstrates a statistically significant upward trend in severe DKA cases requiring intensive care, potentially correlating with healthcare delivery changes or delayed presentations during the COVID-19 pandemic.

This diagnostic imaging panel presents axial brain MRI sequences from a patient with nonketotic hyperglycemic hyperosmolar state (NKHHS). Panels A and B are T2-FLAIR sequences showing multifocal, subcortical hypointensities predominantly in the right hemisphere's white matter. These areas (marked with arrows) demonstrate decreased signal intensity compared to adjacent brain parenchyma. Panel C illustrates Diffusion-Weighted Imaging (DWI), revealing disseminated hyperintense cortical lesions in the right frontal region. Panel D shows the corresponding Apparent Diffusion Coefficient (ADC) map, where these same regions exhibit signal loss (restricted diffusion). The combination of high DWI signal and low ADC signal indicates cytotoxic edema. These findings are characteristic of hyperglycemia-induced brain injury, where metabolic derangement and hyperosmolarity lead to transient neurological deficits and specific neuroimaging patterns, often localized to the subcortical white matter and overlying cortex.

TABLE 13. Hyperosmolar Therapy: Summary of Evidence <table><thead><tr><th>Reference Type of Trauma Center Geographic Location</th><th>Study Design n Age (yr) Outcomes</th><th>Data Class</th><th>Results</th></tr></thead><tbody><tr><td colspan="4">Class 2 studies</td></tr><tr><td colspan="4">Bolus hypertonic saline to control ICP: recommendation II.1.</td></tr><tr><td>Shein et al (2)ᵃ Children's Hospital University of Pittsburgh Pittsburgh, PA</td><td>Prospective n = 16 in analysis Age: mean, 44 mo; range, 34–124 mo ICP and CPP</td><td>Class 2 Differences in patients by treatment, limited control for confounding</td><td>Hypertonic saline vs other drugs for intracranial hypertension Decrease in ICP; increase in CPP Associated with a two-fold faster resolution of intracranial hypertension than either fentanyl or pentobarbital Adjusted hazard ratio, 2.171 (95% CI, 1.062–4.439) Hypertonic saline may be first-line treatment given favorable hemodynamics and resolution of intracranial hypertension. Comparison drugs: beneficial effects on ICP only Fentanyl: ICP decreased; CPP decreased. Highest rate of treatment failure rate Pentobarbital: ICP decreased; CPP no significant change Note: Mannitol not included due to limited use (seven doses out of 362 total; four out 196 analyzed)</td></tr><tr><td>Fisher et al (95) San Diego Children's Hospital San Diego, CA</td><td>RCT n = 18 Age: mean, 8.3; range, 0.6–14.5 ICP</td><td>Class 2 Randomization and allocation concealment methods not reported; crossover study lacking reporting on first-period comparison of baseline characteristics; small sample size</td><td>3% saline vs 0.9% During the 2-hr trial, hypertonic saline was associated with a lower ICP and reduced need for additional interventions (thiopental and hyperventilation) to control ICP. Serum sodium concentration increased ≈7 mEq/L after 3% saline.</td></tr></tbody></table>

Table 1 Continued. <table><thead><tr><th>Hyperglycemia</th><th>French Endocrine Society 2019 (17)</th><th>Hypoparathyroidism</th></tr></thead><tbody><tr><td></td><td>HbA1c GADA, IA2A, ZnT8A Lipase</td><td>n/a</td></tr><tr><td></td><td>IDSC 2018 (18)</td><td></td></tr><tr><td></td><td>Autoantibodies (GADA, IA, islet-cell ZnT8A) Insulin and c peptide</td><td>n/a</td></tr><tr><td></td><td>British Society for Endocrinology 2018 (acute setting) (19)</td><td></td></tr><tr><td></td><td>Monitor and manage for diabetic ketoacidosis or hyperglycemic hyperosmolar state Pancreatic antibodies (e.g. GADA) C-peptide</td><td>n/a</td></tr><tr><td></td><td>ASCO 2018 (10)</td><td></td></tr><tr><td></td><td>If type 1 diabetes suspected: pH, urine ketones, GADA, IA2A, IAA Insulin and c-peptide levels can assist</td><td>n/a</td></tr><tr><td></td><td>SITC 2017 (78)</td><td></td></tr><tr><td></td><td>Blood or urine ketones Tests for antibodies (GADA, IAA, anti-islet cell, ZnT8A) Insulin and c peptide</td><td>n/a</td></tr></tbody></table>

This diagnostic image is an axial slice of a brain MRI, specifically utilizing Diffusion-Weighted Imaging (DWI) or a similar high-contrast sequence to identify acute pathology. The image displays the cerebral hemispheres with visible sulci and gyri and centrally located, hypointense (dark) lateral ventricles. A focal, hyperintense (bright) signal abnormality is identified in the right hemisphere, specifically localized to the head of the caudate nucleus adjacent to the frontal horn of the lateral ventricle. This lesion is highlighted by a blue arrow and is clinically consistent with an acute lacunar infarct. The image is used to demonstrate the localization of small vessel ischemic strokes in patients presenting with encephalopathy or focal neurological deficits, particularly in the context of metabolic derangements like Hyperosmolar Hyperglycemic Syndrome (HHS).